RAAS-mediated cachexia occurs through angiotensin II, which reduces food intake and increases skeletal muscle proteolysis (Fig. 2) by perturbing multiple mediators: increasing interleukin (IL)−6, glucocorticoids, corticotropin-releasing hormone, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation while decreasing insulin-like growth factor 1 (IGF-1), orexin, and neuropeptide Y [7, 61]. The gene discussed is IGF1; the disease is Cachexia.