Notably, the author also observed that macrophage with SORT1-deficiency embraced protective function which inhibited the process of atherosclerosis through suppressed LDL-C uptake and foam cells formation within macrophage [44], indicating a new mechanism of sortilin in regulating the intercellular lipid metabolism aside from the traditional endocytosis of LDL-C in macrophages, such as via the LDLR or via the macropinocytosis. The gene discussed is LDLR; the disease is atherosclerosis.