The various mechanisms that disrupt pRB activity in tumor cells include the loss or silencing of Cyclin-Dependent Kinase (CDK) inhibitors, CDKN2A-D (p15, p16, p18, and p19)7,8, amplification or over-expression of CDK49, 610 or Cyclin D1 (CCND1)11–14, direct mutation the RB1 gene15–17, or expression of viral oncoproteins that target pRB18,19. Here, RB1 is linked to neoplasm.