Whereas, the growth of some cancers, such as colorectal carcinoma and breast cancer, may be restrained by GBP1 activity, GBP1's pro-survival effects can also be hijacked by common oncogenic mutations, such as EGFRvIII, to supercharge its anti-apoptotic effects while the activity of other cooperating factors, such as PIM1 or p38-MAPK, drown out any latent GBP1 anti-proliferative activity and result in an aggressive, TXR+ cancer phenotype. This evidence concerns the gene GBP1 and breast cancer.