Evolution of AML blasts following PD-1 blockade. (A-B) Differentially expressed genes in AML blasts calculated from imputed gene activity scores based on scATAC-seq (A) or from gene expression obtained through scRNA-seq (B). Timepoints include transient partial response to nivolumab (C2D1, C4D1) and subsequent disease progression with unsuccessful re-exposure to nivolumab (relapse, C6D1, and progression). (C) UMAP representation and clustering (scATAC-seq) of AML cells (n = 20 148) with progenitor-like (Pro), megakaryocytic (Mega), and erythroid (Ery) features and relative abundance of clusters over the clinical course. (D) Imputed gene activity scores of GATA2, KLF1, FLI1, and PD-L1 from scATAC-seq data used for annotation of AML cell clusters (C). (E) Chromatin accessibility of CD274 gene (encoding PD-L1 protein) across AML subclusters. (F) PD-L1 expression projected from scRNA-seq data onto scATAC-seq AML subclusters. Statistical testing using Wilcoxon rank sum test. (G) Expression of PD-L1 on AML blasts measured with CyTOF at different timepoints.