Overall, our findings, along with current knowledge, provide a critical link between autophagy dysregulation and prolonged NRF2 signaling in a p62-dependent manner and add some new information that could be useful to explain, at least in part, the close relationship of NPY and macrophages with the pathophysiological mechanisms underlying arteriosclerotic cardiovascular disease [26,27,28], as well as the contradictory results obtained in animal models of atherosclerosis deficient for NPY [30] or NRF2 [72,73,74,75,76]. This evidence concerns the gene NFE2L2 and atherosclerosis.