Because complete suppression of SOCE in human patients with loss of function mutations in ORAI1 and STIM1 genes and mice with abolished SOCE in T cells is prone to severe infections and autoimmunity because of impaired functions of effector T cells and Treg cells, respectively, therapeutic CRAC channel inhibition for IBD would have to be confined to a therapeutic window. This evidence concerns the gene ORAI1 and inflammatory bowel disease.