Although this is the first evidence reporting the involvement of GPR55 in macrophage-to-foam cells formation with an impact on atherosclerosis, our findings seem to be supported by recent reports showing that GPR55 does regulate other cardiovascular-related phenomena, including food intake and adiposity [52–54], glucose-stimulated insulin secretion [55], and platelet and endothelial function [56, 57]. The gene discussed is GPR55; the disease is atherosclerosis.