In contrast, knockdown of p53 in NB-4 cells had no significant influence on apoptosis (Supporting Information Fig. 5A) and cell cycle profile (Supporting Information Fig. 5B), indicating that under basal conditions mutant p53 (C176F) is inactive to execute its tumor suppressor functions but the treatment with FK866 triggers the acetylation of p53 and restores its activity in NB-4 cells. This evidence concerns the gene TP53 and neoplasm.