AKT1 and fibrosis: Additionally, TGF-β1 also leads to cardiac fibrosis through activating several noncanonical (also called Smad-independent) signaling pathways, like phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase [MAPK, mainly comprising p38, c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK)] or Rho-like GTPases signaling pathways.