Abstract
Targeting coinhibitory receptors on dysfunctional T cells may improve response to anti-PD-(L)1 in the IFNγ associated T-cell-inflamed tumor microenvironment. The bispecific lymphocyte activation gene 3 (LAG-3) and PD-L1 blocking antibody FS118, potentially through LAG-3 shedding, represents a promising strategy to improve immune checkpoint blockade. Soluble LAG-3 is an intriguing biomarker for LAG-3 drug activity. See related article by Yap et al., p. 888.