The downregulation of p53 or a significant loss of function—especially as a characteristic of the mutant phenotype—appeared to prevent this regulation, causing FBL overexpression and modulating FBL activity at known methylation sites, which correlated with increased tumorigenesis and colony-forming capabilities in breast cancer tumors via increased FBL and IGF1R-embedded IRES, a noncanonical initiator of protein translation whose expression is necessary for FBL-induced proliferation [133,137]. Here, FBL is linked to breast carcinoma.