Regarding Orai1, several mutations are present in TM domains forming the channel pore or in concentric rings surrounding the pore (G97C, G98S, V107M, L138F, T184M, P245L) [2,3,118,123,128] and induce a constitutively active Orai1 protein, and an increased SOCE mechanism contributing to TAM pathogenesis [2]. Here, ORAI1 is linked to transient myeloproliferative syndrome.