Functional inactivation induced by somatic mutations (mostly nonsense and frameshift) and copy number (CN) deletion of the retinoblastoma tumor suppressor gene (TSG) (RB1), which encodes the retinoblastoma protein (RB), is commonly identified among diverse cancer types [1, 2, 3], resulting in dysfunction of cell cycle progression via deregulation of the activity of E2F transcription factors and promotion of subsequent tumor‐related gene expression [4]. The gene discussed is RB1; the disease is neoplasm.