Consistent with reduced pro‐inflammatory cytokine production by SOCE‐deficient T cells isolated from mice with IBD, we also observed that genetic or pharmacologic inhibition of SOCE suppressed the production of IFNγ and IL‐17A in murine Th1 and T17 cells, respectively, in vitro in a dose‐dependent manner. The gene discussed is IL17A; the disease is inflammatory bowel disease.