RICTOR is a core component of mechanistic target of rapamycin complex 2 (mTORC2), where it functions as a molecular adapter essential for growth factor signaling. mTORC2 phosphorylates and activates AGC protein kinase family members, including AKT, PKC, and SGK1, mediating AKT activation through phosphorylation at serine 473, which facilitates full kinase activation by PDK1. Unlike mTORC1, mTORC2 is nutrient-insensitive and maintains rapamycin resistance through RICTOR. The complex regulates actin cytoskeleton remodeling by activating Rho GTPases and promoting stress-fiber formation, processes critical for cell migration and morphogenesis. RICTOR dysregulation contributes to multiple malignancies and developmental disorders. In chr5 lymphocytic leukemia, ibrutinib treatment induces compensatory upregulation of the FoxO1/RICTOR/mTORC2 axis, driving AKT activation and cell survival 1. In pancreatic ductal adenocarcinoma, mTORC2 cooperates with mTORC1 to activate the Arp2/3 complex, promoting actin-based morphogenesis underlying early transformation 2. Gain-of-function RICTOR variants cause intellectual disability and neurodevelopmental disorders with diverse features including seizures and brain anomalies 3, while a rare RICTOR p.I116V gain-of-function variant predisposes to obesity by enhancing AKT-mediated adipogenesis 4. Therapeutic strategies targeting RICTOR/mTORC2 show promise; in neuroendocrine prostate cancer, pyrvinium pamoate effectively suppresses tumor growth 5, and combination approaches with PI3K/AKT/mTOR inhibitors enhance efficacy in hepatocellular carcinoma.