Similarly, many cancers exhibit aberrant lipid accumulation in tumor DCs [271] thanks in part to excess uptake of exogenous lipids via scavenger receptor A (CD204) [272], excess lipid synthesis by acetyl-CoA carboxylase-1 (ACC-1) [271], and through extracellular vesicle shuttling of lipids from cancer cells to DCs [264]. The gene discussed is ACACA; the disease is neoplasm.