Jia et al. (2020) demonstrated that arsenic-exposed hepatocytes increased altered mitophagy, leading to the generation of mtROS and ox-mtDNA, which culminates in IL-1β, and IL-18 increases, and a glucose metabolism disorder occurs (Figure 2). They demonstrated that the use of a specific scavenger for mtROS (named TEMPO) resulted in the downregulation of mitophagy and ox-mtDNA, inhibited NLRP3 inflammasome activation, and the basal protein expression of NLRP3 and IL-1β in in arsenic-exposed hepatocytes (Jia et al., 2020). Here, IL1B is linked to glucose metabolism disease.