LAUSR

Adaptive resistance mediated by inhibitory ligands such as PD-L1 has emerged as an important mechanism of malignant cell survival and spurred the development of new agents that disrupt the PD-L1/PD-1 immune checkpoint.1 Analysis of patient specimens from clinical trials of novel immune checkpoint inhibitors indicates that high basal expression of PD-L1 on tumor cells may predict sensitivity to and be necessary to elicit significant clinical benefit from this drug class.2, 3 These data suggest that strategies that increase PD-L1 levels could potentially prime malignant cells with low PD-L1 expression and render them sensitive to anti-PD-1/PD-L1 blockade. In order to investigate this possibility, we first conducted an analysis of basal PD-L1 transcript levels in multiple myeloma (MM) patients