Somatic mutations in key proto‐oncogenes or tumour suppressors such as Ras, APC and P53 have been proposed to play a tumour‐initiating role.4 In addition, many studies have shown that aberrant O‐glycosylation of proteins and lipids, resulting in exposure of the immature truncated O‐glycans such as Tn antigen,5, 6 is associated with tumorigenesis and malignant transformation in many human cancers including CRC,7 pancreatic cancer,8 breast cancer,9 liver cancer10 and ovarian cancer.11 The gene discussed is TP53; the disease is neoplasm.