Since Rictor is induced by TGF-β in IPF lung fibroblasts and Akt (Ser473) phosphorylation is an mTORC2 target, we surmised that mTORC2 is a downstream target of TGF-β in IPF fibroblasts; therefore, we turned to examine if blocking mTORC2 inhibits TGF-β-mediated induction of an activated fibroblast or myofibrolast phenotype, which is characterized by the induction of alpha smooth muscle actin (α-SMA) and matricellular proteins such as fibronectin, type I collagen, and secreted protein acidic and rich in cysteine (SPARC), also known as osteonectin. This evidence concerns the gene AKT1 and idiopathic pulmonary fibrosis.