Tumor-associated EndMT is primarily driven by TGF-β/SMAD signaling in concert with inflammatory cytokines and pro-angiogenic cues, accompanied by transcriptional and epigenetic reprogramming that generates EndMT-derived cancer-associated fibroblasts and reinforces an immune-evasive, pro-fibrotic tumor microenvironment [69,94,120,121]. This evidence concerns the gene TGFB1 and cancer.