The possible explanations were that miR-497 not only accelerated cardiomyocyte proliferation and repressed inflammatory responses via targeting multiple genes (including mitofusin 2 and sirtuin 4) but also decreased FGF-23 to inhibit the local renin–angiotensin–aldosterone system, thereby repressing the cardiac hypertrophy and fibrosis in HER2-positive breast cancer patients. Here, MFN2 is linked to hypertrophy.