Growing evidence indicates that MYC mitigates replication stress by induction of homologous recombination repair, upregulation of replication factors (MCM10, WEE1, etc.), cooperation with fork remodelers, and fine‐tuning of RNA polymerase dynamics.[70] It was recently reported that MYC‐dysregulated cancers have an increased dependence on regulators of R‐loop formation to preserve genomic stability, and this vulnerability can be exploited by inhibiting TOP1, a regulator of R‐loop by DNA topology. The gene discussed is MCM10; the disease is cancer.