Nonetheless, high uptake tumors lacking KRAS mutations had higher KRAS signaling scores than KRAS-mutant tumors with low uptake, highlighting a central role of cholesterol uptake on the regulation of KRAS signaling.<h4>Conclusion</h4>In summary, cholesterol uptake emerges as a conserved driver of tumor aggressiveness and a promising therapeutic target to synergize with immunotherapy and KRAS inhibition. The gene discussed is KRAS; the disease is neoplasm.