The contribution of the PI3K/protein kinase B (PKB/AKT) signalling pathway to both fibroblast proliferation and differentiation into myofibroblasts is prominent as fibroblasts isolated from IPF patients have been demonstrated to display pathological activation of AKT [61] and pan-inhibition of upstream class I PI3Ks by the small molecule LY294002-abrogated TGF-β-induced proliferative effects as well as α-SMA expression and collagen production in lung fibroblasts in vitro and bleomycin-induced lung fibrosis in rats in vivo [62,63]. Here, TGFB1 is linked to pulmonary fibrosis.