Together with the finding that ACAC deletion or blockade reduces Th1-mediated inflammation in experimental colitis (29) and limits excessive IFN-γ production in human autoimmunity (30), these aspects contextualize the increased demand for fatty acid synthesis with superior execution of effector functions, including IFN-γ production, in spike- and CEF-specific CD3– T cells. This evidence concerns the gene ACACA and colitis.