Changes in Ca2+ signaling and homeostasis promote the pathophysiology of HCM, affecting the heart’s contractile function and propensity for arrhythmias.[27] Furthermore, the PI3K/Akt pathway affects the behavior of fibroblasts and the production of extracellular matrix proteins, leading to fibrosis, which is frequently observed in HCM. The gene discussed is AKT1; the disease is Arrhythmia.