Diplas et al. found that a subset of isocitrate dehydrogenase (IDH)- and TERTp-wild-type GBM utilized distinct genetic mechanisms of telomere maintenance driven by alternative lengthening in telomerase-positive cells displaying alterations in ATRX or SMARCAL1 and TERT structural rearrangements.21 However, for TERTp-wild-type GBM, there is relatively less information, and the mechanism of telomere maintenance remains unknown. The gene discussed is SMARCAL1; the disease is glioblastoma.