Although the impact of FABP4/FABP5 on atherosclerosis was shown to be mainly due to actions in macrophages [11, 60], cell-based coculture experiments with adipocytes and macrophages and bone marrow transplantation using wild-type and Fabp4−/−Fabp5−/− mice showed that FABP actions in both adipocytes and macrophages have distinct roles in modulation of insulin sensitivity through inflammatory and metabolic responses as shown in Figure 1 [21]. This evidence concerns the gene INS and atherosclerosis.