Moreover, inverse translation studies in mice also showed a trend to lower levels Cd163‐PBL in diet induced mildly hypercholesterolaemic animals, and Cd163‐expression was highly up‐regulated in mice lacking Lrp5, suggesting a direct relationship between high LRP5 and low CD163 levels in macrophages of FH patients. This evidence concerns the gene CD163 and familial hyperaldosteronism.