Owing to the technical difficulties in maintaining bona fide IDH-mutant cells in culture [11], numerous studies have resorted to cell models harboring either CDKN2A/B homozygous deletion or inactivated TP53 and RB1 tumor-suppressor genes, including the “normal human astrocytes” (NHA), which are transduced with the human papillomavirus 16 E6/E7 oncoproteins to block p53 and pRB signaling [12], and the glioblastoma U-87MG cell line, which harbors CDKN2A/B homozygous deletion and PTEN loss [13]. The gene discussed is RB1; the disease is neoplasm.