Thus, neoplastic aggression had a strong impact on amino acid homeostasis even before the onset of cachexia, and progression to cachexia was associated with activation of adaptive mechanisms involved in regulating amino acid availability and utilization in the spleen and liver, including mTORC1 and eIF2α-ATF4 signaling pathways, presumably to cope with the sharp increase in (1) cell growth and (2) positive-APP production, respectively, in these organs. The gene discussed is ATF4; the disease is Cachexia.