In most tissues the leukocyte response to inflammatory stimuli takes place in postcapillary venules (1). Leukocytes and endothelial cells undergo a coordinated and stereotyped series of increasingly tight adhesive interactions designed to capture leukocytes from the bloodstream (2⇓⇓–5). This process generally culminates in migration of leukocytes across the endothelial cells lining the postcapillary venules en route to the site of inflammation. Some notable exceptions occur in specialized capillary beds, such as those that supply the pulmonary alveoli (6, 7) and those that comprise the renal glomerulus (8, 9). Hickey and colleagues recently used intravital microscopy to study the behavior of neutrophils and monocytes in murine glomeruli in the presence and absence of inflammation (9). The authors reported that neutrophils and monocytes normally spend extended periods of time (several minutes) stationary or crawling slowly within the renal capillary lumen. In the presence of local inflammatory stimuli, the duration of these interactions (dwell time) increased and the leukocytes showed signs of intravascular activation (9). In PNAS the group takes these observations to the next level, providing some mechanistic insight into these phenomena (10). The Finsterbusch et al. study sheds some light on how the inflammatory response is regulated in the glomerulus, and also raises some interesting questions for future research. First, the monocytes that spend time interacting with the glomerular capillaries are overwhelmingly the “nonclassical” subset (10). These cells, sometimes called “patrolling monocytes,” are best referred to by the surface markers that they display when isolated. In the mouse, these cells express high levels of the fractalkine receptor CX3CR1 and low or undetectable levels of the chemokine receptor CCR2 and the myeloid marker Ly6C, and are referred to as CX3CR1hi CCR2− Ly6C−. In contrast, “classical” monocytes, sometimes called … [↵][1]1Email: wamuller{at}northwestern.edu. [1]: #xref-corresp-1-1