The pro‐trophic role of melusin has been extensively investigated for cardiac myocytes, where melusin absence accelerates eccentric left ventricle remodelling and transition toward heart failure, whereas melusin overexpression leads to compensatory hypertrophy with increased pump function and protects from dilation.16 Our findings in unloaded skeletal muscle confirm melusin pro‐trophic role and show its relevant contribution to contractility. This evidence concerns the gene ITGB1BP2 and heart failure.