Panier et al. showed that the loss of SLX4IP in U2OS osteosarcoma cells triggered an increase in several markers of ALT, including the formation of ALT-associated promyelocytic leukaemia bodies (APBs), telomeric DNA damage, telomere length heterogeneity, extrachromosomal c-circles and telomeric sister chromatid exchanges (Panier et al., 2019). The gene discussed is SLX4IP; the disease is osteosarcoma.