STIM1 and benign neoplasm: Conversely, increased glucose uptake in the hypertrophic heart also leads to glucose-mediated post-translational modifications of proteins (e.g., O-GlcNAcylation) [167,168], and it is observed that O-GlcNAcylation of STIM1 attenuates SOCE in neonatal cardiomyocytes [169], which could be a feedback pathway to downregulate “overactivated” STIM1 in cardiac hypertrophy (Figure 4➆), while the situation might be converse in diabetic cardiomyopathy.