For example, in cells with altered PI3K signaling, such as cancer cells or pathologic IPF fibroblasts, mTORC1 inhibition may allow uninhibited mTORC2 activity, further suppressing mTORC1 but increasing phosphorylation of AKT and its downstream transcription factors, thus promoting cell survival and proliferation [78,95]. Here, AKT1 is linked to idiopathic pulmonary fibrosis.