Although loss of CGI-58 in macrophages results in comparable TG accumulation, several results were different between CGI-58−/− and ATGL−/− macrophages: Absence of ER stress, mitochondrial apoptosis, and mitochondrial dysfunction, as well as M1-like polarization of CGI-58−/− macrophages, and differences in atherosclerosis susceptibility argue for different and/or additional function(s) of CGI-58 in macrophages beside activation of ATGL. This evidence concerns the gene ABHD5 and atherosclerosis.