MELK was proven to be associated with mitotic progression and DNA damage.8, 9, 10, 11, 12, 13 Kig et al confirmed that MELK was required for the repair of DNA damage (including double‐strand breaks, DSBs) in unperturbed replication.30 Squatrito et al reported that the loss of ATM/Chk2/p53 pathway components accelerated tumour development and contributed to radiation resistance in gliomas.32 In this study, the down‐regulation of MELK restrained the repair of DSBs and led to the continuous phosphorylation of ATM and CHK2. The gene discussed is ATM; the disease is glioma.