AKT1 and neoplasm: LUAD has been demonstrated to remotely reprogram hepatic insulin, glucose, and lipid metabolism through STAT3-Socs3 pathway-mediated alterations in proinflammatory responses that disrupt AMPK, Akt, and SREBP signaling.225 Furthermore, subcutaneously implanted lung cancer cells activate the hypothalamic‒pituitary axis to secrete α-melanocyte-stimulating hormone (α-MSH), which has been shown to promote MDSC generation through MC5R receptor signaling in bone marrow precursor cells, ultimately enhancing tumor growth.226