The latter effect seemed dominant in untransformed cells, illustrating the tumor suppressor role associated with KLF4. Changing the cell's genetic background by introducing an oncogenic RasV12 allele not only abolished the cytostatic function of KLF4 through bypassing CDKN1A induction, but switched it into an oncogenic effect, with KLF4 showing its dominant action on repressing TP53 and thus preventing apoptosis. This evidence concerns the gene KLF4 and neoplasm.