The article discusses the challenges in developing animal models for neuropsychiatric disorders such as schizophrenia, depression, and bipolar disorder. These disorders are complex, with symptoms that are subjective and lack objective diagnostic tests. Despite this, animal models are crucial for understanding pathophysiology and developing treatments. However, current models have limitations in validation and predictive power for human disease. The authors argue that creating more useful models requires focusing on areas with clearer genetic links and using validated methods. They emphasize the importance of construct, face, and predictive validity in evaluating models. For schizophrenia, models based on genetic mutations or environmental factors have shown some promise, but their validity remains debated. For depression, models involving chronic stress or HPA axis disruption have been used, but their face validity is questionable. For bipolar disorder, models involving psychostimulants or genetic mutations have been developed, but their construct validity is limited. The authors suggest that future models should focus on replicated risk alleles, chronic environmental manipulations, and a broad range of behavioral assays. They also recommend that authors clearly state the goals of their models and the types of validity applied. Overall, while animal models are valuable, they are unlikely to fully replicate human disorders, and their use should be guided by clear scientific criteria.The article discusses the challenges in developing animal models for neuropsychiatric disorders such as schizophrenia, depression, and bipolar disorder. These disorders are complex, with symptoms that are subjective and lack objective diagnostic tests. Despite this, animal models are crucial for understanding pathophysiology and developing treatments. However, current models have limitations in validation and predictive power for human disease. The authors argue that creating more useful models requires focusing on areas with clearer genetic links and using validated methods. They emphasize the importance of construct, face, and predictive validity in evaluating models. For schizophrenia, models based on genetic mutations or environmental factors have shown some promise, but their validity remains debated. For depression, models involving chronic stress or HPA axis disruption have been used, but their face validity is questionable. For bipolar disorder, models involving psychostimulants or genetic mutations have been developed, but their construct validity is limited. The authors suggest that future models should focus on replicated risk alleles, chronic environmental manipulations, and a broad range of behavioral assays. They also recommend that authors clearly state the goals of their models and the types of validity applied. Overall, while animal models are valuable, they are unlikely to fully replicate human disorders, and their use should be guided by clear scientific criteria.