We previously showed that SOCE is essential for pathogenic Th17 cell function as mice with T cell‐specific deletion of ORAI1, STIM1 or STIM2 were protected in Th17 cell‐dependent animal models of autoimmune diseases such as EAE and colitis (Ma et al, 2010; McCarl et al, 2010; Schuhmann et al, 2010; Kaufmann et al, 2016). Here, STIM2 is linked to colitis.