Inhibition of STAT3 leads to regression of the hypertrophic pathologies in the heart (Mir et al., 2012), whereas cardiac hypertrophic responses are noted as a result of overexpression of STAT3 in cardiomyocytes in vivo (Kunisada et al., 2000), supporting cell-autonomous effects of activated STAT3 in cardiac hypertrophy. Here, STAT3 is linked to cardiac hypertrophy.