The release of IL-11 by fibroblasts and epithelial cells plays a pivotal role in fibroblast stimulation, myofibroblast differentiation, and extracellular matrix deposition, facilitated by both Smad-independent mechanisms and the PI3K/Akt pathway [68, 69].Thus, targeting these fibrotic mediators or signaling pathways may represent a promising therapeutic strategy for combating fibrotic diseases, including kidney stones associated with diabetes. This evidence concerns the gene AKT1 and nephrolithiasis.