New immune signatures emerge from differently expressed genes between PLXNC1^high/low and IDO1^high/low samples. (A) Kaplan-Meier estimates of OS according to the signature composed by the top 20 DE genes between PLXNC1^high/low samples in the TCGA-AML cases (median used as cutoff, P < .05). (B) Kaplan-Meier estimates of OS according to the signature composed by the top 20 DE genes between IDO1^high/low samples in the TCGA-AML cases (median used as cutoff, P < .01). (C) Kaplan-Meier estimates of OS according to the signature composed by the top 3 DE genes (IKBKB, FOSL1, and TLR9) between PLXNC1^high/low samples in the TCGA-AML cases (median used as cutoff, P < .0001). (D) Kaplan-Meier estimates of OS according to the signature composed by the top 4 DE genes (GZMH, GNLY, IFIT2, and IFIT3) between IDO1^high/low samples in TCGA-AML cases (median used as cutoff, P < .05). (E) Kaplan-Meier estimates of OS according to the signature composed by the top 3 DE genes from the PLXNC1^high/low signature (IKBKB, FOSL1, and TLR9) and the top 4 DE genes from IDO1^high/low signature (GZMH, GNLY, IFIT2, and IFIT3) in the TCGA-AML dataset (median used as cutoff, P < .01). (F) Representation of genetic alterations of the 7 DE genes deriving from the PLXNC1^high/low and IDO1^high/low signatures (IKBKB, FOSL1, TLR9, GZMH, GNLY, IFIT2, and IFIT3) in the TCGA-AML dataset. (G) Comparison of frequency of mutations between samples with abnormalities (mRNA high/low) vs without abnormalities of the 7 DE genes derived from the PLXNC1^high/low and IDO1^high/low signatures (IKBKB, FOSL1, TLR9, GZMH, GNLY, IFIT2, and IFIT3). (H) Kaplan-Meier estimates of OS according to the signature composed by the integration of the 7 DE genes derived from the PLXNC1^high/low and IDO1^high/low signatures (IKBKB, FOSL1, TLR9, GZMH, GNLY, IFIT2, and IFIT3) with the IDO1, BIN1, and PLXNC1 genes in the TCGA-AML dataset (median used as cutoff, P < .0001).