TP53 and neoplasm: In support of this molecular mechanism, it has been reported that human tumor-derived p53 mutants, whose TAD was inactivated by site-directed mutagenesis, lost the ability to increase tumorigenicity in vitro and in vivo [8,13, 19-21]; (b) recent work by Di Agostino et al. has shown that mutant p53 proteins physically interact in vivo with the transcription factor NF-Y, whose DNA binding consensus are present in the regulatory regions of many key genes involved in the regulation of the cell cycle.