Taken together, the key findings of our study suggesting that the silencing of ANRIL can result in suppressed invasion and proliferation, while acting to enhance the apoptosis of retinoblastoma cells by up-regulating the ATM-E2F1 signaling pathway, thus providing a fresh basis for which the treatment of retinoblastoma may be premised upon. The gene discussed is CDKN2B-AS1; the disease is retinoblastoma.