Recent research from many laboratories highlighted important connections between hemopoiesis and allergy / asthma. Hemopoiesis in an allergic inflammation site differs greatly from steady-state (homeostatic) hemopoiesis in the bone-marrow, due to differences in the hemopoietic factors present, as well as on their targets. One major aspect concerns the role of GM-CSF, which seems unnecessary for steady-state hemopoiesis in the absence of infection, but plays a central role in the immunobiology of the lungs, especially in the instructive phase of imunity, by its ability to influence dendritic cell differentiation and function. Allergens, alone or in combination with other factors, can induce GM-CSF production in the airways, and therefore bypass the requirement for microbial products in the activation of dendritic cells. Hemopoietic progenitors and dendritic cell precursors recruited to the lung provide additional potential targets for GM-CSF. Stem Cell Factor also plays a major role, by acting on mast cells to promote their maturation and functional activation, and on additional cell types from the lung to promote allergic inflammation, in concert with IgE antibodies and a variety of chemokines. Hemopoietic cells isolated from bone-marrow, blood and allergic lung may differ in their responses to hemopoietic factors and drugs. This is changing our perception of the effects of glucocorticoids on hemopoiesis, and especially on eosinophil differentiation. Manipulation of the process of granulocyte (eosinophil and neutrophil) apoptosis, as well as engineering modified versions of hemopoietic cytokines, such as IL-5, are current approaches to developing valuable tools for intervention in the context of hemopoiesis in allergy.