For example, similar co-occurrence patterns that have been shown to collaborate in model organisms consist of alterations in KRAS and TP53 in pancreatic cancer, ERG translocations and PTEN deletions in prostate cancer, APC and KRAS in CRC, or MYC and TP53 in various cancer types (4, 30–34). This evidence concerns the gene TP53 and familial pancreatic carcinoma.