Several pathways are activated in renal fibrosis: (1) AT1R induction of p38-MAPK and JNK signaling induces TGF-β activation, which contributes to an epithelial–mesenchymal cell transition [108]; (2) EGFR activation by the Ang II–AT1R axis also activates TGF-β, which leads to renal fibrosis [109]; (3) Ang II–AT1R via NF-κB pathway induces various inflammatory effectors (IL-6, TNF-α) that affect inflammatory responses [108]. This evidence concerns the gene IL6 and renal fibrosis.