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. Here, MYD88 is linked to Obesity.