The key findings of other articles included (1) macrophage Aldh1a2, a gene involved in the metabolism of retinoic acid, was depressed with anti-miR-33 treatment, resulting in the activation of Treg and protection against atherosclerosis (67); and (2) netrin-1 as a neuronal guidance cue that mediates chemorepulsion and chemoreattraction of axons through receptor UNC5b, promotes atherosclerotic plaque progression through the retention of macrophages within inflamed blood vessels (68). Here, NTN1 is linked to atherosclerosis.