Similar results were obtained after aphidicolin, γ-irradiation or cisplatin treatment in U-2OS cancer cell line (Supplementary Material, Fig. S3D–G), which survive through a telomerase-independent alternative lengthening of telomeres (ALT) mechanism (reviewed in 2,36), thus indicating that neither mutations compromise NHP2’s role in DNA damage response. This evidence concerns the gene NHP2 and cancer.