IL3 and Alzheimer disease: They find that (i) a subpopulation of astrocytes secrete the classical cytokine interleukin-3 (IL-3), (ii) microglia are responsive to this cytokine, (iii) responsiveness (not so much secretion of IL-3) is increased in patients with AD and model systems of AD, and (iv) presence of IL-3 is necessary to allow microglia to counteract some of the detrimental effects of AD: if IL-3 is missing, AD pathology worsens (see Fig. 1 for graphical depiction).1