Confirming that this is the result of chronic STAT activation, they proved that Gal-1-mediated impact on PD-L1 and Gal-9 in the tumour endothelium promotes T-cell exclusion, as Gal-1 blockade significantly boosted T-cell infiltration and conferred enhanced response to immunotherapy (109). The gene discussed is LGALS1; the disease is neoplasm.