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. This evidence concerns the gene AKT1 and cardiac arrhythmia.