The regulation of muscle differentiation is indeed dependent on the activation of signal transduction cascades with the complex involvement of key kinases, such as the serine/threonine kinase Akt, and previous studies demonstrated that Akt is essential to promote protein synthesis and cell survival and to block protein degradation [13], All this evidence supports its biological relevance in the context of cachexia. The gene discussed is AKT1; the disease is Cachexia.