Notably for the hypothesis that B cells play a central role in maintaining steady-state haematopoiesis, B lymphopoiesis is itself compromised in autoimmunity and ageing (47) where chronic IL-1R/TLR4 signalling stimulates HSC proliferation and drives the proinflammatory myeloid/lymphoid bias (16, 48–50) by promoting (i) preferential development of myeloid cells from HSCs and dendritic cells from common lymphoid progenitors; (ii) induction of apoptosis of developing B cells and (iii) egress of developing B cells from the BM (48, 49). The gene discussed is TLR4; the disease is Autoimmunity.