Marcovecchio et al. (2017) recently showed that CD36 is essential for the function of nonclassical monocytes by regulating patrolling activity during early stage of atherosclerosis. The adaptor protein DAP12 and SFKs facilitate the patrolling function, and deleting CD36 in these cells decreased oxLDL uptake and significantly reduced patrolling speed and distance. Interestingly, deleting a different scavenger receptor, SR-A, did not reduce oxLDL uptake or numbers of patrolling cells, but SR-A deficient cells had defects in patrol speed and distance (Marcovecchio et al., 2017). The gene discussed is CD36; the disease is atherosclerosis.