STIM1 and cardiac hypertrophy: Studies by Molkentin and colleagues (Correll et al., 2015) showed that cardiomyocyte-specific overexpression of STIM1 not only resulted in increased Ca2+ entry but also promoted cardiac hypertrophy, decreased cardiac function, increased mortality, and increased fetal gene expression which was associated with mitochondrial ultrastructural abnormalities and significant alterations in Ca2+ handling (i.e., spontaneous Ca2+ transients, increased Ca2+ spark frequency, increased diastolic Ca2+, and remodeling of the L-type Ca2+ channel (LTCC) current).