Phosphoinositide 3‐kinase gamma (PI3Kγ) catalyzes the production of phosphatidylinositol‐3,4,5‐triphosphate by phosphorylating phosphatidylinositol (PI), phosphatidylinositol‐4‐ phosphate (PIP) and phosphatidylinositol‐4,5‐bisphosphate (PIP2). Catalytic subunit of PI3Kγ is activated by βγ subunits of heterotrimeric G proteins in response to chemokines, growth factors and hormones, which in turn coordinates cell migration, cell growth, cell cycle entry, and cell survival. PI3Kγ has been implicated in T cell function, but direct effect of its kinase function has not been evaluated. Using mice expressing a catalytically inactive mutant of PI3Kγ(PI3KγKD/KD) we were able to demonstrate that defect in kinase activity leads to T cell developmental defect in the thymus and results in decreased peripheral T cell numbers. PI3KγKD/KD peripheral CD4 and CD8 T cells demonstrated impaired TCR/CD28‐induced proliferation and IL‐2 production, reduced chemokine driven chemotaxis and impaired T cell differentiation. Thus, our study demonstrated that kinase activity of PI3Kγ amend status of T cell response by contributing to thymic development, T cell activation and differentiation as well as lymphocyte chemotaxis.