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]. This evidence concerns the gene CAMK2G and cardiac hypertrophy.