a RNA-seq was performed on primary BMMs in the presence of IFNγ, and/or FK866, and NMN. GSEA signatures for inflammatory and glycolysis pathways, showing the enrichment of genes whose IFNγ-dependent induction is lowered in the presence of the FK866 NAMPT inhibitor treated BMMs. b The same GSEA pathways showing rescue of FK866-dependent inhibition by NMN. For a, b, NES normalized enrichment score, padj adjusted p value: two-tailed, corrected for multiple comparisons using Benjamini–Hochberg method. c RT-qPCR expression of indicated inflammatory genes in the presence of FK866 under LPS/IFNγ stimulation. d Flow cytometry measurement of mean fluorescence intensity for CCR1 abundance on the cell surface in the presence of the indicated treatments. e IL-6 cytokine secretion into culture medium after 24 h treatment with indicated conditions as measured by ELISA, and quantified using purified standard dilutions. f NO secretion measured by Griess assay of nitrite levels in culture medium in the same conditions as in e. For c–f, results presented are the average of N = 3 biological replicates, and are representative of at least three independent experiments. p values were determined by a two-tailed unpaired t-test: *p < 0.05, **p < 0.005, ***p < 0.0005, ****p < 0.00005. Error bars represent SEM.