Bi et al. reported that global inhibition of UCHL1 using heterozygous germ-line Uchl1 knockout or a pharmacological compound (LDN-57444) attenuated TAC-induced cardiac hypertrophy, fibrosis, and LV malfunction in mice and, conversely, overexpression of UCHL1 via recombinant serotype 9 adeno-associated viruses (rAAV9)-mediated gene delivery exacerbated the pathology (20). Here, UCHL1 is linked to cardiac hypertrophy.