Vulval differentiation in Caenorhabditis elegans is controlled by a conserved signal transduction pathway mediated by Ras and a kinase cascade that includes Raf, Mek and MAPK. Activation of this cascade is positively regulated by a number of proteins such as KSR (kinase suppressor of Ras), SUR‐8/SOC‐2, SUR‐6/PP2A‐B and CDF‐1. We describe the functional characterization of sur‐7 and several genes that regulate signaling downstream of ras. We identified sur‐7 by isolating a mutation that suppresses an activated ras allele, and showed that SUR‐7 is a divergent member of the cation diffusion facilitator family of heavy metal ion transporters that is probably localized to the endoplosmic recticulum membrane and regulates cellular Zn2+ concentrations. Genetic double mutant analyses suggest that the SUR‐7‐mediated effect is not a general toxic response. Instead, Zn2+ ions target a specific step of the pathway, probably regulation of the scaffolding protein KSR. Biochemical analysis in mammalian cells indicates that high Zn2+ concentration causes a dramatic increase of KSR phosphorylation. Genetic analysis also indicates that PP2A phosphatase and PAR‐1 kinase act downstream of Raf to positively and negatively regulate KSR activity, respectively.