To establish a tumor model with restoring of p16INK4A expression in an acute manner to avoid a potential complication of a long-term stable expression of p16INK4A-induced senescence, we restored p16INK4A expression in DFBM-Ni17 tumor cells in an inducible fashion (referred as DFBM-Ni17/tetp16INK4A). This evidence concerns the gene CDKN2A and neoplasm.