Mutated p53 not only lost its anti-cancer effects but might also exhibits various GOF activities, which promote tumor proliferation, migration, metabolic reprogramming, and immune escape, influencing tumor epithelial-mesenchymal transition (EMT), immune checkpoints (such as PDL1), and stemness markers (such as CD44) through sigaling pathways such as EGFR, AMPK, and NF-κB (58–60). The gene discussed is NFKB1; the disease is neoplasm.