CD11b⁺ myeloid progenitor cells, originating from the bone marrow, migrate to the site of inflammation to promote angiogenesis and lymphangiogenesis. Several possible mechanisms are listed here. (1) Release of cytokines and growth factors with proangiogenic activity, including VEGF. (2) Production of proteases such as the cysteine protease cathepsin and matrix metalloprotease-9 (MMP-9), which mediate degradation of the extracellular matrix and release of VEGF from its membrane-bound form. (3) Myeloid cell differentiation into endothelial cells, a mechanism that is still debated. (4) Direct interaction between myeloid cells and blood or lymphatic endothelial cells through CEACAM1 in an homophilic manner, as described by Horst et al in the article that begins on page 6726. Professional illustration by Debra T. Dartez.