Cibi et al. (2020) observed the development of hypertrophic cardiomyopathy in aged mice with a cardiac-null mutation of Prdm16 (Prdm16flox/flox; Mesp1-Cre) [13], which experience progressive cardiac dysfunction by echocardiography, as evidenced by decreased left ventricular ejection fraction (LVEF); fractional shortening (FS); and increased end-systolic volume (ESV), end-diastolic volume (EDV), and left ventricle internal diameter during end-systole (LVIDes) [13]. This evidence concerns the gene PRDM16 and hypertrophic cardiomyopathy.