TAM has been predominantly linked to mutations in the genes encoding (i) stromal interaction molecule-1 (STIM1) and (ii) calcium release-activated calcium (CRAC) channel ORAI1, which are two proteins that mediate a mechanism known as Store-Operated Ca2+ entry (SOCE) [3,5,6,7,8,9,10]. The gene discussed is ORAI1; the disease is transient myeloproliferative syndrome.