Gene inactivation by homologous recombination is a relatively new tool to become available to the fly community, which Sears et al. have put to good use on p. 3557 to inactivate Pvr, which encodes a receptor tyrosine kinase of the PDGF/VEGF family and is required for hemocyte/macrophage migration. By examining loss-of-function Pvr mutants, created by both gene targeting and chemical mutagenesis, the authors have discovered that Pvr is required for fly CNS morphogenesis – in its absence, axon scaffold formation and glial mispositioning defects occur in the CNS. By studying two other fly mutants with similar CNS defects – serpent, which lacks hemocytes, and flies mutant for the macrophage scavenger receptor,Croquemort – the authors conclude that the CNS defects of Pvrmutants are caused by the failure of macrophages to engulf cell corpses within the CNS, leading to disrupted glial and axon positioning.