DNA replication stress (RS) is a term that broadly defines DNA replication disorders, and usually refers to events that cause replication forks to slow down or stall. The excessive accumulation of replication stress is the main driver of tumorigenesis and genome instability. Cell chromosomes constantly expose to exogenous or endogenous replication stress in replication, telomeres and common fragile sites are some chromosome regions that are highly sensitive to replication stress. These regions are usually difficult to completely replicate under high replication stress. Recent studies have found that mitotic DNA repair synthesis (MiDAS) is different from S phase replication, which can help difficult-to-replicate regions to be able to replicate after entering mitosis. Therefore, MiDAS is also called “rescue mechanism of replication”. Since the maintenance of telomeres depends on telomerase activity and alternative lengthening of telomeres (ALT), ALT cells have more fragility of telomeres, and MiDAS shows high levels of activity, so this reviews the mechanism of MiDAS and how difficult-to-replicate telomeres respond to replication stress to complete DNA synthesis during mitosis under different telomere maintenance mechanisms.