miR-146a limits inflammaging in human AML. (A) GSEA plots showing enrichment of inflammaging pathway target gene expression in aged vs young primary AML patient samples in this study’s AML cohort and in the TCGA adult AML cohort. (B) GSEA plot showing enrichment of inflammaging pathway target gene expression in aged vs young, normal CD34⁺ cells (microarray data from Pang et al³⁷ ). (C) Number of miRNA genes significantly anticorrelated (Spearman’s false discovery rate [FDR]–adjusted P < .01) with inflammaging pathway target gene expression in this study and the TCGA cohort. (D) Ranking of overlapping miRNA candidates from panel C that were predicted to bind to >2 inflammaging pathway target genes. Ranking is based on the average rank of predicted seed sequences in inflammaging pathway target transcripts. Better-ranking candidates have lower average and overall rank scores. (E) Kaplan-Meier survival analysis of AML patients (this study’s cohort) with low (bottom tertile) vs high (top tertile) miR-146a expression. P by log-rank. (F) GO term EnrichmentMap of the largest gene expression network upregulated in miR-146a low vs miR-146a high AML. EnrichmentMap cutoffs: FDR <0.075; P < .005, and overlap >.75. AutoAnnotate network labels: Markov cluster analysis of GO term names. (G) GSEA hallmark gene sets upregulated in miR-146a low vs miR-146a high AML in this study and the TCGA cohort (normalized enrichment score [NES] >1.5). (H) GSEA plots showing enrichment of cytokine signaling hallmark gene sets in genes upregulated in miR-146a low vs miR-146a high AML.