On the one hand, targeting CD98hc downregulates tumour growth by decreasing the redox counterbalance capacity mediated by CD98hc-xCT116,117, by limiting the required balance in the AA content for proper protein synthesis and cell proliferation, mostly harmonised by CD98hc-LAT1118–122, and by compromising integrin-regulated signalling pathways4,5,13. This evidence concerns the gene SLC3A2 and neoplasm.