Dr Méndez-Ferrer gained his PhD in Medical Physiology in 2004 at the University of Seville (Spain).  From 2006-10, he worked as post-doc and Research Assistant Professor at Mount Sinai School of Medicine in New York, USA. His work led to the discovery that hematopoietic stem cell (HSC) traffic is regulated by circadian oscillations and identified self-renewing mesenchymal stem cells that have a crucial role in the HSC niche. Dr. Mendez-Ferrer has been a PI since 2010, and based in Cambridge since 2015. His current research focuses on the regulation of the HSC niche in health and disease.  HSCs reside in specialised niches, which allows them to self-renew, proliferate, differentiate and migrate according to the organism's requirements. His research has revealed multisystem regulatory mechanisms by which the HSC niche fulfils these complex functions and how the deregulation of these mechanisms contributes to haematological disorders. His research has discovered a connection between the bone marrow, the brain and other systemic signals, which regulate the behaviour of HSCs. His work has received international attention manifested in 13 Plenary presentations at international meetings and 150 invited presentations.  It has been recognized with several awards (ASH Scholar Award, Joanne Levy Memorial Award, HHMI International Early Career Scientist), has generated international publications in top journals (Nature, Cell Stem Cell) and 3 patent applications. His translational research has fructified into two Phase-II multicentre clinical studies currently testing the possible redeployment of mirabegron (a beta3-adrenergic agonist) and tamoxifen to modulate the HSC niche in myeloproliferative neoplasms. He is Chair of ASH Scientific Committee on Hematopoiesis, Reviewing Editor of eLife and Training Director of the Cambridge Canter Centre. He has been Associate Editor of Haematologica. Ongoing efforts in his lab are targeting the microenvironment to improve bone marrow transplantation procedures and as a complementary therapeutic target for the treatment of myeloid malignancies.