However, high expression of Δ40p53 in Δ40p53-lentivirus-infected melanoma cells was shown to activate endogenous p53 and form Δ40p53/p53 heterotetramers that alter promoter occupancy of apoptotic gene PIDD and cell-cycle arrest gene p21, thereby promoting apoptosis over cell-cycle arrest upon γ-irradiation [172]. The gene discussed is TP53; the disease is melanoma.