Alternatively, one may hypothesize that CHC could enhance vascular wall inflammatory responses and lead to atherosclerosis by activeing NLRP3 inflammasomes, which regulate caspase-1 activation and subsequent processing of pro-IL-1β, triggering IL-1 secretion38, a processes inhabitable by DHI whereas the secretion of IL-10 is reduced in NLRP3−/− macrophage, which implying that NLRP3 inflammasomes activation may contribute to IL-10 secretion93, a process independent of DHI regulation. This evidence concerns the gene IL1B and atherosclerosis.