Mechanistical studies suggested that metabolic stress-induced activation of the PI3K/AKT pathway was the underlying cause since the chemical inhibitors of the PI3K pathway, LY294002 and Wortmannin, relieved the inhibition of the IFNy-STAT1 signaling pathway, resulting in restored antigen presentation, and restored CD8 T cell recognition of the tumor cells. The gene discussed is CD8A; the disease is neoplasm.