LATS2 is an endogenous regulator of cardiac hypertrophy during TAC [95]; in detail, Matsui et al. suggested that in response to PO, there was an upregulation of endogenous LATS2, which increased cardiomyocyte MST1-mediated apoptosis and inhibited adaptive cardiac hypertrophy [95]. Here, MST1 is linked to cardiac hypertrophy.