When this finding is considered in the context of a recently identified transcription factor (TCF3/E2A) that increases expression of p21 while decreasing that of p53 target PUMA, a mediator of p53-induced apoptosis, (Andrysik et al., 2013) it seems possible that there may be an imbalance present in some molecular subtypes of CRC toward p21 activation and cell cycle arrest vs. PUMA activation and apoptosis. This evidence concerns the gene TP53 and colorectal carcinoma.