The latest research progress by Li's group suggested that miR-27b-3p deficiency remarkably reduced cardiac hypertrophy, fibrosis, and inflammation in both TAC and Angiotensin II (Ang II) perfusion-induced murine models; surprisingly, inhibition of endogenous miR-27b-3p could significantly enhance mitochondrial oxidative phosphorylation (OXPHOS) through activating PGC1α/β (65). The gene discussed is AGT; the disease is cardiac hypertrophy.