In contrast to our in vitro findings, where TTFields exposure of IL-4-polarized M2 macrophages reduced Arg1 and increased MHC-II/CD80 and pro-inflammatory mediators consistent with an M1-like shift, the in vivo data show a different pattern: in the orthotopic lung cancer model, TTFields significantly increase iNOS in both CD206− (M1-like) and CD206+ (M2-like) TAMs, but do not reduce Arg1 frequency or MFI in CD206+ TAMs or in total macrophages. This evidence concerns the gene CD80 and lung cancer.