In a mouse model of MC38 colon carcinoma, Tang et al. demonstrated that targeting the tumor with an anti-EGFR antibody fused to mutated LIGHT protein (optimized for binding to the mouse lymphotoxin-beta receptor (LTβ-R) and herpes virus entry mediator (HVEM) receptor and for preventing the spontaneous aggregation of the recombinant LIGHT molecule) enhanced T-cell anti-tumor response and contributed to overcome resistance to PD-L1 blockade by facilitating HEV induction and T-cell tumor infiltration via CD68+ macrophages activation (88). Here, EGFR is linked to neoplasm.