Several investigations have revealed a loss of SERCA2 isoform b (SERCA2b) expression and activity in islets (Cardozo et al., 2005; Kono et al., 2012), heart (Wold et al., 2005; Takada et al., 2012), and liver (Park et al., 2010; Fu et al., 2011) in selected models of diabetes, suggesting that SERCA2 dysfunction is a potential pathology for development of diabetic complications. Here, ATP2A2 is linked to diabetes mellitus.