In contrast, the activation of IFN-β signaling pathway in KTRMs using IL-37b not only suppresses cyst formation but downregulates the pro-inflammatory factors such as CXCL1 and CXCL4, demonstrating the therapeutic potential of metabolic-immune interaction regulation in the autosomal dominant polycystic kidney disease (ADPKD) (100). This evidence concerns the gene CXCL1 and autosomal dominant polycystic kidney disease.