Kelley’s research in the Walsh lab within the Molecular Biology and Biochemistry Department is centered on elucidating the role of DRAK2 signaling in T lymphocyte metabolism. Clonal expansion of T cells is often essential for effective immune responses, but in order to avoid lymphoproliferative disease and autoimmunity, negative regulation of T cell activation is crucial. The serine/threonine kinase DRAK2 is a negative regulator of T cell receptor (TCR) signaling. A loss of this kinase leads to an altered threshold for activation, allowing T cell proliferation under suboptimal stimulation conditions. Despite enhanced T cell activation, Drak2-/- mice are resistant to experimental autoimmune encephalomyelitis (EAE). However, the basis for this autoimmune resistance is currently unknown. Emerging evidence highlights an intimate correspondence between cellular metabolism and immunity. Of note, T cell activation via TCR stimulation results in extensive metabolic reprogramming, a process required to meet the biosynthetic demands of rapid clonal expansion. The bioenergetic profile adopted by specific T cell subsets depends on a variety of factors including the type of activation and the substrate availability within the environment. Our results show that, in the absence of DRAK2 signaling, T cells exhibit selective alterations in metabolic profile, leading to differential transcriptional and translational responses. These findings demonstrate that DRAK2 is selectively important for T cell metabolism and highlight the potential that DRAK2 modulation of metabolic activity may serve as an attractive therapeutic target for the treatment of autoimmune diseases.