ISP has been demonstrated to induce cardiac hypertrophy, and fibrosis is attributed to the involvement of PTEN/AKT/mTOR pathway, a downstream signaling pathway known for its role in pathological conditions, including cardiac hypertrophy and fibrosis, where the downregulation of PTEN and the phosphorylation of AKT/mTOR play a role in the pathogenesis of cardiac hypertrophy and fibrosis and the reversal of which would act as a protection against both cardiac hypertrophy and fibrosis.32 The gene discussed is AKT1; the disease is cardiac hypertrophy.