Therefore, we transformed RPTECs into a pro-inflammatory and pro-fibrotic disease state (designated as CK+) by stimulating the cells with cytokines (IL-1β, OSM, and TGF-β1) that are implicated in the development of phenotypes also observed in CKD (e.g., inflammation and fibrosis).79 The gene discussed is TGFB1; the disease is glycogen storage disease VI.