Li et al. reported that endothelial-monocyte-activating polypeptide II (EMAP 2), a tumor-derived pro-inflammatory cytokine, promoted autophagic vacuole formation and inhibited the PI3K/AKT/mTOR signaling pathway, thereby inducing autophagy and inhibiting the viability, migration, and angiogenesis of GB (77). The gene discussed is PIK3CA; the disease is neoplasm.