It has recently been reported that GCN2 is a key driver of the induction of anti-inflammatory macrophage functional polarization and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment, depending on ATF4 and altered oxidative metabolism and myeloid-lineage deletion of GCN2 can changes in the immune microenvironment with increased proinflammatory activation of macrophages and MDSCs and IFNγ expression in intratumoral CD8+ T cells [6]. The gene discussed is EIF2AK4; the disease is neoplasm.