Cell cycle checkpoints are stringent quality control mechanisms that regulate cell cycle progression and division. Cancer cells often develop a dependency on the G2/M cell cycle checkpoint to facilitate DNA repair and resolve intrinsic or therapy-induced DNA damage. This dependency leads to therapy resistance, continuous cell division, and disease progression. Targeting G2/M checkpoints has been heavily pursued over the past two decades and has progressed into clinical studies. Recent genome-scale functional genomic studies have revealed that Myt1 kinase, an essential but previously overlooked molecule for the G2/M checkpoint, is a promising target for multiple types of cancers. In this work, we summarize the latest discoveries in molecular targeting of Myt1 kinase and discuss the challenges and limitations in expanding its clinical application.

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