Conversely, BIRC5 knockdown induced G1 cell cycle arrest and increased apoptotic activity, accompanied by activation of checkpoint pathways.<h4>Conclusion</h4>This study defines BIRC5 as a cell-state-specific regulator of malignant proliferation in retinoblastoma and provides a mechanistic rationale for targeting survivin in highly proliferative tumor subpopulations. Here, BIRC5 is linked to neoplasm.