CPT1A and neoplasm: In our study, targeting the blockade of CPT1A by Eto dramatically reduced the SLC7A11 and ARG1 gene and protein expression in MDSCs in vitro and in vivo in the tumor microenvironment, leading to not only enhancing IKE-induced MDSC actual ferroptotic death and blocking MDSCs’ immunosuppressive function but also strengthening T-cell proliferation (Figure 3) and infiltration into tumor tissues, thus, ultimately, promoting IKE-triggered tumor growth inhibition (Figure 4).