Specifically, RIPK3 candirectly phosphorylate CaMKII or indirectly oxidize CaMKII through ROS, whichpromotes the opening of the mitochondrial permeability transition pore (MPTP),increases mitochondrial membrane permeability, decreases mitochondrial membranepotential, inhibits the mitochondrial oxidative phosphorylation reaction, andpromotes ROS production, ultimately causing necroptosis in cardiomyocytes andpromoting pathological cardiac hypertrophy [82]. The gene discussed is RIPK3; the disease is cardiac hypertrophy.