Recent advances have established that the inflammatory adaptation of haematopoietic stem and progenitor cells (HSPCs) towards myeloid-biased haematopoiesis constitutes a main driver of long-lived trained innate immunity. The latter represents an epigenetically based memory state that leads to elevated inflammatory preparedness to future infectious or inflammatory challenges.1 This inflammatory memory is passed on epigenetically from HSPCs to progeny myeloid cells (‘trained’ or hyper-responsive neutrophils and monocytes).