STIM1 gain‐of‐function mutations induce SOCE overactivity and give rise to TAM/STRMK [5], while loss of STIM1 accompanied by SOCE failure impairs extracellular Ca2+ entry and causes severe combined immunodeficiency (SCID), characterized by chronic infections, autoimmunity, muscular hypotonia and ectodermal dysplasia [22, 23]. This evidence concerns the gene STIM1 and ectodermal dysplasia syndrome.