To counteract this inflammatory state, the pathway of the anti-inflammatory cytokines interleukin-4 (IL-4), interleukin-10 (IL-10) and interleukin-13 (IL-13) is activated inducing the stress response of the hypothalamic-pituitary-adrenal axis, which in turn induces an increase in cortisol synthesis that will cause secondarily, and as unwanted side effects, bone resorption, lipolysis, protein catabolism, gluconeogenesis and immune dysfunction, depending on the system on which it acts, ultimately producing frailty and sarcopenia. This evidence concerns the gene IL10 and sarcopenia.