Stuttering is a complex speech disorder that occurs in early childhood during a critical phase of brain and behavioral development. Recent studies have identified early brain changes linked to stuttering, while spontaneous recovery is associated with increased inter-area connectivity. Therapy-driven improvement in adults is linked to functional reorganization within and beyond the speech network. However, the etiology of stuttering remains unclear. This Unsolved Mystery highlights critical questions and neuroimaging findings that could inspire future research to understand how genetics, neural hierarchies, social context, and reward circuits contribute to stuttering. Stuttering is a speech disorder where speakers know what they want to say but experience intermittent loss of control, leading to speech blocks, sound repetitions, and prolongations. It can severely limit interpersonal communication and impact education and employment. Stuttering onset occurs between ages 2 and 5, with up to 8% of preschoolers beginning to stutter, and about a fifth retaining it into adulthood. Stuttering is characterized by intermittency and variability, with symptom severity varying across days, weeks, and months. It is also influenced by personality, social context, and emotional state. Genetic research suggests a complex genetic architecture for stuttering, with heritability studies showing higher concordance in monozygotic twins. However, environmental factors also play a role. The sex bias in stuttering, with a higher prevalence in males, suggests sex-related neurobiological factors may influence recovery. Genetic studies have linked stuttering to rare variants in lysosomal targeting pathway genes and novel chromosomal loci. However, genome-wide association studies have not replicated previously identified loci, indicating limited success in identifying genetic factors. Neuroimaging studies have shown that stuttering is associated with atypical brain structure and function, including differences in cortical and subcortical motor structures. Persistent stuttering is linked to reduced gray matter volume in the left ventral premotor cortex and subcortical areas, as well as white matter differences. Spontaneous recovery in children is associated with increased white matter growth and normalization of brain structures. Adults with stuttering show increased neural activity in the basal ganglia, including the putamen and caudate nucleus. Stuttering therapy in adults can lead to neural reorganization, with interventions such as fluency training and brain stimulation enhancing speech fluency. However, complete recovery is rare, and relapse is common. Neuroimaging studies suggest that stuttering therapy can lead to normalization of brain activity and improved connectivity between speech-related brain regions. The singing advantage is a notable phenomenon, as singing can significantly reduce stuttering. This may be due to differences in neural control of the larynx, with the dorsal laryngeal motor cortex involved in pitch regulation. The ventral laryngeal motor cortex is associated with articulatory voicing and is weakened in individuals who stutter. Social context plays a significant role in stuttering, with symptoms worsening in communicativeStuttering is a complex speech disorder that occurs in early childhood during a critical phase of brain and behavioral development. Recent studies have identified early brain changes linked to stuttering, while spontaneous recovery is associated with increased inter-area connectivity. Therapy-driven improvement in adults is linked to functional reorganization within and beyond the speech network. However, the etiology of stuttering remains unclear. This Unsolved Mystery highlights critical questions and neuroimaging findings that could inspire future research to understand how genetics, neural hierarchies, social context, and reward circuits contribute to stuttering. Stuttering is a speech disorder where speakers know what they want to say but experience intermittent loss of control, leading to speech blocks, sound repetitions, and prolongations. It can severely limit interpersonal communication and impact education and employment. Stuttering onset occurs between ages 2 and 5, with up to 8% of preschoolers beginning to stutter, and about a fifth retaining it into adulthood. Stuttering is characterized by intermittency and variability, with symptom severity varying across days, weeks, and months. It is also influenced by personality, social context, and emotional state. Genetic research suggests a complex genetic architecture for stuttering, with heritability studies showing higher concordance in monozygotic twins. However, environmental factors also play a role. The sex bias in stuttering, with a higher prevalence in males, suggests sex-related neurobiological factors may influence recovery. Genetic studies have linked stuttering to rare variants in lysosomal targeting pathway genes and novel chromosomal loci. However, genome-wide association studies have not replicated previously identified loci, indicating limited success in identifying genetic factors. Neuroimaging studies have shown that stuttering is associated with atypical brain structure and function, including differences in cortical and subcortical motor structures. Persistent stuttering is linked to reduced gray matter volume in the left ventral premotor cortex and subcortical areas, as well as white matter differences. Spontaneous recovery in children is associated with increased white matter growth and normalization of brain structures. Adults with stuttering show increased neural activity in the basal ganglia, including the putamen and caudate nucleus. Stuttering therapy in adults can lead to neural reorganization, with interventions such as fluency training and brain stimulation enhancing speech fluency. However, complete recovery is rare, and relapse is common. Neuroimaging studies suggest that stuttering therapy can lead to normalization of brain activity and improved connectivity between speech-related brain regions. The singing advantage is a notable phenomenon, as singing can significantly reduce stuttering. This may be due to differences in neural control of the larynx, with the dorsal laryngeal motor cortex involved in pitch regulation. The ventral laryngeal motor cortex is associated with articulatory voicing and is weakened in individuals who stutter. Social context plays a significant role in stuttering, with symptoms worsening in communicative