IRAK3 and essential thrombocythemia: This correlation suggests a more nuanced role for HIF1α in ET, where it not only upregulates IRAK-M expression in monocytes but also concurrently downregulates pro-inflammatory cytokine production and monocyte reprogramming (44), leading to the immunosuppressive phenotype and enhanced protective functions characteristic of ET such as phagocytosis, anti-microbial activity, and tissue remodelling (32, 37).