The TGF-β family, including TGF-β and bone morphogenetic proteins (BMPs), plays a crucial role in the biology of glioblastoma (GBM), the most common malignant brain tumor in adults. TGF-β signaling promotes tumorigenesis by inducing cancer stem cell (CSC) self-renewal, tumor cell migration, and immune system suppression, while BMPs suppress tumorigenic potential by inducing tumor cell differentiation. The review discusses the actions of TGF-βs and BMPs on cancer cells and the tumor microenvironment, highlighting their potential as therapeutic targets. TGF-β signaling is activated through the binding of ligands to type II and type I receptors, leading to the activation of SMAD proteins and the induction of target genes. BMPs also bind to these receptors, activating R-SMADs and forming complexes with SMAD4 to translocate to the nucleus. Both TGF-β and BMP signaling pathways are involved in various cellular processes, including proliferation, migration, and apoptosis. In GBM, high levels of TGF-β are associated with poor prognosis, and its activity is modulated by deubiquitinating enzymes. TGF-β promotes GBM progression by inducing proliferation, invasion, and self-renewal, while BMPs have tumor suppressor roles, inducing differentiation and blocking proliferation. The tumor microenvironment, characterized by immunosuppression and dynamic extracellular matrix alterations, is influenced by TGF-β and BMPs. Therapeutic approaches targeting TGF-β signaling, such as neutralizing antibodies and small-molecule inhibitors, have shown promise in preclinical and clinical trials. However, the complex nature of these signaling pathways poses challenges in their effective use as therapeutic targets.The TGF-β family, including TGF-β and bone morphogenetic proteins (BMPs), plays a crucial role in the biology of glioblastoma (GBM), the most common malignant brain tumor in adults. TGF-β signaling promotes tumorigenesis by inducing cancer stem cell (CSC) self-renewal, tumor cell migration, and immune system suppression, while BMPs suppress tumorigenic potential by inducing tumor cell differentiation. The review discusses the actions of TGF-βs and BMPs on cancer cells and the tumor microenvironment, highlighting their potential as therapeutic targets. TGF-β signaling is activated through the binding of ligands to type II and type I receptors, leading to the activation of SMAD proteins and the induction of target genes. BMPs also bind to these receptors, activating R-SMADs and forming complexes with SMAD4 to translocate to the nucleus. Both TGF-β and BMP signaling pathways are involved in various cellular processes, including proliferation, migration, and apoptosis. In GBM, high levels of TGF-β are associated with poor prognosis, and its activity is modulated by deubiquitinating enzymes. TGF-β promotes GBM progression by inducing proliferation, invasion, and self-renewal, while BMPs have tumor suppressor roles, inducing differentiation and blocking proliferation. The tumor microenvironment, characterized by immunosuppression and dynamic extracellular matrix alterations, is influenced by TGF-β and BMPs. Therapeutic approaches targeting TGF-β signaling, such as neutralizing antibodies and small-molecule inhibitors, have shown promise in preclinical and clinical trials. However, the complex nature of these signaling pathways poses challenges in their effective use as therapeutic targets.