TMPRSS11D and persistent truncus arteriosus: Recently, HAT and histone deacetylase (HDAC) were shown to be involved in the modulation and regulation of hypertrophic responses in heart dysfunction.4, 5, 6 We previously demonstrated that the imbalance of histone acetylation modification induced by HAT is involved in the development and progression of cardiac hypertrophy and that anacardic acid (AA) can decrease alcohol‐mediated cardiac hypertrophy.7 Unfortunately, the mechanism of AA underlying the Chinese herb extract‐mediated attenuation of cardiac hypertrophy caused by transverse aortic constriction (TAC) remains unclear.