Our data suggest that the downregulation of Smad-independent TGF-β1 signaling, as well as the p38 MAP kinase and Akt pathways, by ApoSQ-exposed CM inactivates transcription factors that bind to the Snai1/2, Zeb1/2, and Twist1 promoters in the tumor microenvironment and consequently results in preventing EMT progression.31 Indeed, we found that apoptotic cancer cell-exposed CM inhibits the migration and invasion of lung cancer cells. This evidence concerns the gene AKT1 and lung cancer.