Hence, methylation was essential for cardiomyocyte homoeostasis and hypertrophy.90 Likewise, the histone trimethyllysine demethylase, JMJD2A, promoted cardiac hypertrophy in response to hypertrophic stimulation in mice and induced an increase in the expression of hypertrophy markers including B‐type natriuretic peptide and natriuretic peptide A in pluripotent stem cell‐derived cardiomyocyte (Table 5).91, 92 The histone demethylase, PHF8, was also observed to attenuate cardiac hypertrophy upon cardiac overload 93 (Figure 3). The gene discussed is KDM4A; the disease is cardiac hypertrophy.