Zhao et al. observed that Akt activation in human cardiac fibroblasts (HCF) and rats (C57BL/6) caused myocardial fibrosis via the myocardial infarction–associated transcript (MIAT), resulting in increased IL-1β, IL-6, and TNF-α mRNA levels and numerous proteins that collectively contribute to the onset of heart failure (50). This evidence concerns the gene AKT1 and Myocardial fibrosis.