This study demonstrated that blocking CPT1A by etomoxir sodium salt (Eto) augments imidazole ketone erastin (IKE)-induced MDSC actual ferroptotic death and blocks MDSC immunosuppressive function and accumulation by breaking the SLC7A11 and GPX4 ferroptosis defense systems and downregulating the expression of ARG1, which impair tumor growth via promoting T-cell proliferation and infiltration into tumor tissues. The gene discussed is SLC7A11; the disease is neoplasm.