In Yang et al.’s investigation, it was observed that in lung adenocarcinoma, hyperactivated CTLs induce tumor cells to produce prostaglandin E2 (PGE2) and recruit myeloid-derived suppressor cells (MDSCs) via the Fas/FasL signaling axis, thereby fostering tumor immune evasion (67). The gene discussed is FASLG; the disease is neoplasm.