ULK1-induced alternative mitophagy prevents the development of pathological cardiac hypertrophy under pressure overload. The study by Nah et al.¹³ provides evidence to show the cardioprotective effect of ULK1-mediated alternative mitophagy against pressure overload stress (TAC mouse model). In response to pressure overload, ATG7/ATG5-dependent mitophagy is acutely activated but rapidly diminished after 1 day. Conversely, ULK1/Rab9-mediated alternative mitophagy is activated and sustained for several days following TAC, actively clearing defective mitochondria. Moreover, the myocardium of the mice deficient for ULK1 (ULK1cKO) exhibited large dysfunctional mitochondria with poorly defined cristae. Indices of pathological cardiac remodelling such as increased fibrosis, loss of mitochondrial integrity, and cardiac dysfunction were evident. These findings point towards the importance of ULK1-mediated alternative mitophagy in mitochondria clearance and attenuating pressure overload induced cardiac dysfunction.