Cells expressing both c-MYC and PIM showed increased tumor progression, leading to an advanced cancer phenotype, and silencing of PIM1 resulted in c-MYC-related tumor inactivation, suggesting that PIM1 may be required to maintain c-MYC-driven aggressive PCa.37,38 Other downstream PIM targets include p27 (cyclin-dependent kinase inhibitor 1B)39,40 and BAD (Bcl2-associated death promoter).8,41. Here, CDKN1B is linked to neoplasm.