New preclinical work indicates that targeting cholesterol transport enzymes could suppress tumor growth by starving cancer cells of needed lipid trafficking. Researchers reported that blocking PI5P4K-linked cholesterol transport disrupts intracellular lipid movement, creating a “cholesterol traffic jam” that limits growth in experimental models. Separately, researchers at CNIC reported that mitochondrial complex I is a required driver of dendritic cell function, acting like a “mitochondrial checkpoint” for immune activation and improving immunotherapy effectiveness. The mechanistic link connects tumor immunology outcomes to cellular metabolic control points.