Yang et al. successfully switched the telomere lengthening machinery of telomerase-positive cancer cells (HTC75) to an ALT-mediated telomere elongation mechanism by knocking out the TERT, inducing telomeric DNA damage, and disrupting the ATRX/DAXX complex [154], suggesting that ATRX and TERT mutations are mutually exclusive in conferring a selective growth advantage in cancers through telomere maintenance. Here, ATRX is linked to cancer.