In addition, reactiveoxygen species (ROS) are induced under hyperglycemia, subsequently triggering therelease of TXNIP from thioredoxin, activating TXNIP/NLRP3 and a series of relatedinflammatory reactions, and leading to β-cell apoptosis.40, –42 Recently, NADPH oxidase 5(NOX5) was identified as a downstream target of the TLR pathway, and NOX5-derivedROS may be modulated by IRAK.43 Furthermore, ROS activate NLRP3 by promoting TXNIP and NIMA-related kinase 7interactions with NLRP3. Here, IRAK1 is linked to Hyperglycemia.