This overgrowth is driven by increases in cyclooxygenase2-prostaglandin E2 and mTOR [14], and also by a powerful autocrine growth loop involving Transforming Growth Factor-alpha (TGF-α) and its receptor, EGFR, which is potently exacerbated by the hyperphosphatemia of advanced CKD [7,15]. The gene discussed is TGFA; the disease is hyperphosphatemia.