This study demonstrated that blocking CPT1A by Eto augments IKE-induced MDSC actual ferroptotic death and blocks MDSCs’ 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 GPX4; the disease is neoplasm.