The tumor suppressor protein retinoblastoma (RB) is genetically or functionally inactivated in many human cancers, and exerts its tumor-suppressive functions through physical interactions with various effector molecules including E2F transcription factors, tissue-specific transcription factors, LxCxE motif-containing chromatin modifiers, and the E3 ubiquitin protein ligase SKP2. Here, RB1 is linked to neoplasm.