By constructing a panel of syngeneically derived NSCLC cells expressing wild-type (wt-) p53 or various mutant (mut-) p53 that had been shown to be the “hotspot” mutations with Gain-of-Function (GOF) activity on the H1299 cells with p53 deficiency, our current work further validated the observations in the population study that, FOSB served as a tumor suppressor in NSCLC cells expressing wt-p53, while a tumor promoter in those expressing most types of the mut-p53 tested (including p53 deficiency as a special mutation type of TP53) (Fig. 3). Here, FOSB is linked to neoplasm.