Conversely, reintroduction of ATRX into ATRX-null ALT cancer cells restores H3.3 deposition at telomeres, thereby inhibiting sister telomere exchange and causing growth suppression.54 Thus, our finding that small-molecule inhibition of PARP-1 activity attenuated growth of ATRX-deficient cells offers a potentially therapeutic avenue towards treatment of ALT-positive cancers, analogous to PARP-1 inhibitor treatment to eliminate BRCA1/2-deficient cancer cells.58, 59, 60. This evidence concerns the gene PARP1 and cancer.