In addition, FT3 can modulate genes that encode numerous important structural and functional proteins of the myocardium, including myosin heavy chains (encoded by MYH6 and MYH7), sodium/potassium-transporting ATPases, sarcoplasmic/endoplasmic reticulum calcium ATPase 2, and ryanodine channel, etc. Genetic analysis has indicated that mutations in the MYH7 and RYR2 genes might be linked to the pathogenesis of LVNC [37, 38], and the prevalence of MYH7 mutations is the highest among LVNC patients [17]. The gene discussed is ATP2A2; the disease is left ventricular noncompaction.