In light of the parallel relationship between the distinct antithesis in the tumor biological functions of wild-type (wt-) and mutant (mut-) p53 and the opposite prognostic effects of FOSB expression in LUAD and LUSC, we speculated that the mutation status of the TP53 gene might serve as a golden key to unlocking the “two sides” of FOSB in NSCLC. Here, TP53 is linked to neoplasm.