Together with HIPK2 deletion forms, we tested a few point mutants including the tumor-associated N958I and R868W mutants, which have been shown to possess a reduced p53 activation capacity [35], the kinase-defective K228R [36, 37], the sumoylation-resistant K32A [38], the ubiquitylation-resistant K1189R [39], and the non-acetylatable K835R [40]. This evidence concerns the gene TP53 and neoplasm.