Mechanistically, the development of meCAF phenotypes is driven by paracrine signals, such as IL-6, TGF-β, and tumor-derived exosomal miRNAs (e.g., miR-105), which activate the Myelocytomatosis oncogene (MYC) and Ataxia Telangiectasia Mutated (ATM) signaling pathways in fibroblasts, thereby causing metabolic shifts [65]. This evidence concerns the gene ATM and neoplasm.