The RAAS signal is mechanistically coherent: efferent arteriolar vasodilation lowers intraglomerular pressure and narrows the kidney’s autoregulatory reserve, blunting the angiotensin II–mediated response to hypovolemia; under CRT conditions, characterized by emesis, mucositis, reduced oral intake, and episodic dehydration, this hemodynamic milieu increases prerenal ischemia and susceptibility of proximal tubular cells to cisplatin injury [28,29,30]. This evidence concerns the gene AGT and mucositis.