PRRT2 and myocardial infarction: These results show that the PKC–inositol-3-phosphate signaling pathway may be directly involved in inducing cardiac hypertrophy in the right ventricle for maintaining its function upon inducing myocardial infarction, whereas depressed phospholipase C activity as well as its substrate affinity may produce a decrease in the ability of the right ventricle to generate contractile force and limit the hypertrophic response as a consequence of a decrease in the formation of inositol-3-phosphate and subsequent Ca2+ release from the intracellular Ca2+ stores [35].