Neuronal cell migration and axon guidance both require proper regulation of the actin cytoskeleton as the cell responds to several extracellular guidance cues. A member of the small GTPase family Rho/Rac is one of the intrinsic factors in actin remodeling. Similar to other small GTPase families, the GTP-bound form of Rac interacts with effector proteins to be delivered to its appropriate membrane domain and function properly. In C. elegans, the CED-10/Rac functions in the migration of several types of cell and in axon pathfinding in cooperation with the MIG-2 Rho-like GTPase. CED-10 also regulates the phagocytosis of apoptotic cells. However, the precise molecular mechanisms by which CED-10 interacts with its effector proteins and regulates specific cellular responses to guidance cues are not well understood. In this study, we identified RIN-1 as a novel CED-10/Rac effector that is involved in cell migration and axon guidance. Using a constitutive active-form of CED-10 as bait, we performed a yeast two-hybrid screening and found that the C. elegans homologue of Rin1 is physically bound to CED-10. Rin1 was originally identified as a Ras-interacting protein in mammalian cells, but its function in C. elegans has not been reported. In our in vitro assays, the C. elegans RIN-1 protein specifically bound to the GTP-form of CED-10, but not to the CED-10 GDP-form. Furthermore, RIN-1 did not physically interact with other members of the Rho/Rac family, suggesting that RIN-1 may function as a specific effector protein for CED-10. To confirm this, we examined whether rin-1 mutants have similar phenotypic defects with ced-10 or mig-2 mutants. The rin-1 single mutants did not show obvious defects, however, the rin-1; mig-2 double mutants had significantly severe defects in axon pathfinding of the AVM neuron, neuronal cell migration, and dorsal morphology of the body compared to the defects observed in the mig-2 single mutants. This suggests that RIN-1 and MIG-2 act redundantly in actin remodeling during these migration events, which is similar to CED-10 and MIG-2 redundancy. However, we also found that rin-1 is not involved in several CED-10 signaling pathways, such as the migration of the distal tip cells and the phagocytosis of apoptotic cells. Together with genetic analyses using guidance mutants, our results strongly indicate that RIN-1 acts as an effector of CED-10 in specific cells or in actin remodeling in response to a restricted guidance molecule.