Following the latter, in rhabdomyolysis-induced AKI, the treatment with the antioxidant anisodamine decreases inositol-requiring enzyme-1α (IRE-1α), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) and activating transcription factor 4 (ATF4), reducing NLRP3 inflammasome components (i.e., NLRP3, caspase-1, IL-1β and IL-18) [126], suggesting that ROS is implicated in ER-stress protein’s activation. This evidence concerns the gene IL1B and acute kidney injury.