Studies have shown that the PI3K-Akt signaling pathway was directly involved in the formation of IPF or cooperated with other pathways to promote the development of IPF [63], while the TNF signaling pathway was upregulated in bleomycin-induced fibrotic lung tissue and TNF-α-induced NF-κB activation promoted fibroblast differentiation and exacerbated bleomycin-induced pulmonary fibrosis [64]. Here, AKT1 is linked to pulmonary fibrosis.