The latter was explained by the observation that the diabetes-linked mutation of the SEC61A1 tyrosine 344 to histidine affects the di-tyrosine motif-containing mini-helix of the Sec61 α-subunit, i.e., the BiP-binding site (Schäuble et al., 2012; Figures 5, 9).” As a consequence, the mutated Sec61 channel cannot be efficiently gated by BiP and thus becomes permeable for Ca2+. This evidence concerns the gene HSPA5 and diabetes mellitus.