EGFR activation, induced by mutations, has been observed to induce upregulation of glutamine metabolism in some cancer studies.[4, 26] A strategy to inhibit GLS 1 in addition to EGFR block has shown promising anti‐tumor effects in preclinical colon and lung cancer models.[4, 27] Therefore, we hypothesized that tumors with glutamine addiction, might benefit from preferential glutamine inhibition in the TME, and thereby, enhance the efficacy of EVax against EGFR‐driven lung tumorigenesis. Here, EGFR is linked to neoplasm.