We found that perturbation of RRP15-dependent RiBi in p53 proficient non-transformed cells activated the classical impaired ribosome biogenesis checkpoint (IRBC) and induced cell cycle G1-G1/S arrest, while depletion of RRP15 in p53-deficient tumor cells induced S-G2/M arrest and apoptosis via activating the ATR-Chk1-γH2AX axis and DNA replication/damage checkpoint responses [16]. This evidence concerns the gene RRP15 and neoplasm.