In head and neck cancer, tumor-secreted Gal-1 hampers T cell infiltration in the TME by upregulating both programmed death ligand 1 (PD-L1) and Gal-9 and activating the STAT signaling pathway in endothelial cells (ECs), mediating tumor resistance to anti-PD-1 therapy [116]. The gene discussed is SOAT1; the disease is neoplasm.