In contrast, MYDGF conditional transgenic overexpression or MYDGF protein injection can inhibit G protein-coupled agonist-induced hypertrophy and augment Sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA2a) expression in cardiomyocytes by enhancing Pim-1 proto-oncogene serine/threonine kinase (PIM1) expression and activity, thereby attenuating pressure overload-induced ventricular hypertrophy and dysfunction (Korf-Klingebiel et al. 2021). This evidence concerns the gene MYDGF and Ventricular hypertrophy.