The tumor microenvironment further contributes to NSCLC aggressiveness, as senescent fibroblasts in idiopathic pulmonary fibrosis secrete exosomal MMP1, activating PAR1/PI3K-AKT-mTOR signaling to drive cancer proliferation and invasion-a pathway targetable by PAR1 inhibitors [265]. This evidence concerns the gene MTOR and neoplasm.