The mTOR kinase regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2. This study demonstrates that differentiation into T(H1) and T(H17) subsets is regulated by mTORC1 signaling, which depends on the small GTPase Rheb. Rheb-deficient T cells fail to generate T(H1) and T(H17) responses in vitro and in vivo, but retain the ability to become T(H2) cells. In contrast, mTORC2 signaling deletion prevents T(H2) differentiation but allows T(H1) and T(H17) differentiation. These findings identify mechanisms by which mTORC1 and mTORC2 regulate helper T cell fate differently. The study also shows that mTORC1 signaling promotes T(H1) and T(H17) differentiation, while mTORC2 signaling promotes T(H2) differentiation. Inhibition of mTOR leads to the differentiation of regulatory T cells. The study highlights the distinct roles of mTORC1 and mTORC2 in regulating T cell differentiation and their impact on immune responses. The results suggest that mTORC1 and mTORC2 signaling pathways are essential for the proper differentiation of helper T cells and the development of immune responses. The study also demonstrates that the inhibition of both mTORC1 and mTORC2 is required for the generation of regulatory T cells in the absence of exogenous TGF-β. The findings provide a critical link between metabolism and T cell differentiation, highlighting the importance of mTOR signaling in immune function.The mTOR kinase regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2. This study demonstrates that differentiation into T(H1) and T(H17) subsets is regulated by mTORC1 signaling, which depends on the small GTPase Rheb. Rheb-deficient T cells fail to generate T(H1) and T(H17) responses in vitro and in vivo, but retain the ability to become T(H2) cells. In contrast, mTORC2 signaling deletion prevents T(H2) differentiation but allows T(H1) and T(H17) differentiation. These findings identify mechanisms by which mTORC1 and mTORC2 regulate helper T cell fate differently. The study also shows that mTORC1 signaling promotes T(H1) and T(H17) differentiation, while mTORC2 signaling promotes T(H2) differentiation. Inhibition of mTOR leads to the differentiation of regulatory T cells. The study highlights the distinct roles of mTORC1 and mTORC2 in regulating T cell differentiation and their impact on immune responses. The results suggest that mTORC1 and mTORC2 signaling pathways are essential for the proper differentiation of helper T cells and the development of immune responses. The study also demonstrates that the inhibition of both mTORC1 and mTORC2 is required for the generation of regulatory T cells in the absence of exogenous TGF-β. The findings provide a critical link between metabolism and T cell differentiation, highlighting the importance of mTOR signaling in immune function.