Attenuation of cardiac hypertrophy by proteasome inhibitor (bortezomib) in Ang II infused mice was shown to be due to inhibition of degradation of ATIR-associated proteins and inactivation of AT1R-mediated p38 MAPK and STAT3 signaling pathways; this has been suggested to be beneficial for treating pathological cardiac hypertrophy [86]. This evidence concerns the gene AGTR1 and cardiac hypertrophy.