IL1B and kidney disorder: Indeed, during the pathogenesis of kidney disease, mitochondria in damaged cells become one of the main sources of excess ROS, which in turn implements the activation of transcription factors NF-κB, AP-1, and p53, exacerbating the production of pro-inflammatory cytokines and chemokines such as IL-1β, IL-6, IL-8, IL-1, and TNF-α, monocyte chemoattractant protein-1 (MCP-1), interferon-invasive protein-10 (IP-10), molecules of adhesion such as selectin, ICAM, VCAM, ELAM, inflammatory enzymes, such as iNOS and COX-2, and further ROS/RNS [109,110,111,112,113].