TP53 and neoplasm: In this context, the smoker-biased DML reported by Kaz et al. at TNXB (extracellular matrix (ECM)/epithelial–mesenchymal transition (EMT)linkage), GFI1 (p53/Notch repressor), NTRK2/3 (neurotrophin receptors), and CLDN11 (tight junctions) is mechanistically consistent with smoke-induced epithelial remodeling and selective silencing of differentiation/tumor-suppressive pathways [119,147,148,149,151,156,157].