A St. Jude-led study in Science reports that tumors can suppress immune “gatekeeper” dendritic cells by reprogramming their mitochondrial metabolism. In preclinical mouse models, restoring mitochondrial fitness in dendritic cells enhanced immunogenic activity and improved tumor control. The work ties tumor-driven metabolic stress to dendritic cell dysfunction in nutrient-sparse tumor microenvironments. When high-mitochondrial dendritic cells were combined with immune checkpoint blockade, the study found the strongest antitumor effects, including slowed or halted tumor growth and improved survival versus either approach alone. The findings point to a mechanistic lever that could be combined with existing immunotherapies, particularly where checkpoint blockade alone has been less effective.