A novel review highlights the dual role of the tumor suppressor gene CHEK2 in enhancing the efficacy of immune checkpoint inhibitors (ICIs) for solid tumors. CHEK2 deficiency drives increased tumor mutational burden and activates the cGAS-STING pathway, cultivating a pro-inflammatory tumor microenvironment that attracts cytotoxic T cells. This mechanistic insight, emerging from Northwestern University Feinberg School of Medicine, suggests CHEK2 as a promising biomarker and target to amplify immunotherapy responses across cancer patients.