Stanger et al. [46] reported that cell cycle regulation could effectively improve tumor immunosuppression, and that cell cycle progression depended on the coordinated expression and activity of cyclins; cyclin-dependent kinases 4 and 6 (CDK4/6) were particularly promising targets for therapeutic interventions, and the researchers developed CDK4/6 kinase inhibitors which could not only effectively inhibit tumor growth, but also improve the tumor immunosuppressive microenvironment, making it significantly more sensitive to immune checkpoint blockade. The gene discussed is CDK4; the disease is neoplasm.