On the contrary, BLM, WRN, and RTEL1 expression was increased in ATRX KO neuroblastoma cells after the inactivation of p53, leading the authors to suggest that in ATRX‐deficient cells, the other helicases compensate for this loss and allow G4 resolution and replication fork stability [41]. The gene discussed is RTEL1; the disease is neuroblastoma.