MRC1 and glioblastoma: Whereas N3‐methyladenine and N7‐methylguanine are readily repaired by base excision repair (BER), O6‐methylguanine forms DNA mismatches with thymine during replication, triggering a futile cycle of the mismatch repair (MMR) pathway, collapse of the replication fork, and DNA double‐strand breaks.[4] Therefore, GBM cells proficient in MMR respond positively to Tmz therapy, whereas cells lacking MMR machinery tolerate the damage and are resistant to treatment.