SLC3A2 and neoplasm: Targeting SLC3A2 on cancer cells could enhance the ability of immune cells to function in the tumor microenvironment.82 Loss of target expression is a key mechanism of acquired resistance to CAR T cell therapies in the clinic.83 In the case of SLC3A2, we observed that its knock-out in A2058 cancer cells stopped their in vitro proliferation, which is consistent with previously reported data both in vitro and in vivo.66 As a consequence, antigen loss is unlikely to be a resistance mechanism to SLC3A2 targeting as it would result in impaired cell proliferation in cancer cells.