MiR‐133a was down‐regulated in thyroid hormone‐regulated cardiac hypertrophy,37 and miR‐23a acted downstream of NFATc3 to regulate cardiac hypertrophy,38 and overexpression of miR‐27b could induce cardiac hypertrophy.39 Wang reported that miR‐103/107 could regulate programmed necrosis and myocardial ischaemia/reperfusion injury through the FADD pathway.40 However, whether miR‐103 plays a role in cardiac hypertrophy has not been addressed. The gene discussed is FADD; the disease is cardiac hypertrophy.