Because epsins 1 and 2 are paralogs with overlapping expression and function, we focused primarily on epsin 1 for in vitro studies; however, to elucidate the role of endothelial epsins in atherosclerosis, we generated ApoE−/− mice with an endothelial cell-specific deletion of epsin 1 on a global epsin 2 knock-out background (EC-iDKO/ApoE−/−) to circumvent the redundant function of two epsins (Supplementary Fig. 1a, b)18,19,25. The gene discussed is EPN1; the disease is atherosclerosis.