AHR inhibition leads transcriptional reprograming of NK cells. (A) Heatmap showing hierarchical clustering of DEGs between SR-1– and DMSO (control)-expanded NK cells on day 14. RNA isolated from control- or SR-1–expanded NK cells was used for RNA-seq. The transcripts were aligned to the human GRCh38 assembly. The results show the expression of genes that change 1.5-fold (P < .05). Hierarchical clustering was performed using Pearson correlation. (B) Multivariate plot showing the expression of highest expressed gene upregulated or downregulated between the control (DMSO) and SR-1 treatment groups. Each dot represents a gene, with the x axis representing expression and the y axis representing fold change. Dots colored red show genes whose differential expression is considered statistically significant (<10% false discovery rate). (C) Principal component analysis showing the genes from day 14 SR-1– or DMSO-expanded NK cells. x and y axes show principal component 1 (PC1) and principal component 2 (PC2) that explain 92% and 5% of the total variance, respectively. (D) Venn diagram showing the number of AHR targets genes in NK cells expanded with SR-1 as identified by AHR ChIP-seq on day 14. (E) IPA showing the top 10 signaling pathways. Gene ontology analysis was performed using the list of differentially expressed AHR target genes (148) from day 14 SR-1–expanded NK cells.