Given the increasing evidence that LPS-stimulated TLR4/MyD88 signalling is critical in driving both emergency pro-inflammatory myelopoiesis to fight infection and the myeloid/lymphoid skewing associated with (obesity-accelerated) ageing (66), our working model is that ES-62 harnesses its ability to subvert TLR4 signalling and downregulate MyD88 in order to counteract such dysregulation of HSCs, both in the BM and the periphery. The gene discussed is MYD88; the disease is infection.