Regarding classical oncogenes and tumour suppressors in GI cancers, we found no difference in TP53 and KRAS mutations, while APC mutations were less common (7.1% vs 35.5%, p<0.001) and ERBB2 amplifications more common (16.4% vs 7.5%, p=0.001) in case of MTAP loss, again likely due to the low prevalence of CRC and high prevalence of GEC in this population. This evidence concerns the gene TP53 and colorectal carcinoma.