Vulva1 induction in C. elegans is controlled by a highly conserved signaling pathway similar to the RTK-Ras-MAPKcascade in mammals. By screening for suppressors of the Multivulva phenotype caused by an activated let-60 ras allele, we isolated mutations in a gene, ksr-f, that acts as a positive modifier of vulva1 induction and is required for at least two other let-60 rasmediated processes. Although ksr-7 mutations do not perturb vulva1 induction in an otherwise wild-type background, they have very strong effects on vulva1 induction in genetic backgrounds where Ras pathway activity is constitutively activated or compromised, suggesting that ksr-7 activity is required for maximal stimulation of vulva1 fates by the Ras pathway. Genetic epistasis analysis suggests that ksr-1 acts downstream of or in parallel to let-60 ras. We cloned ksr-7 and have shown that it encodes a novel putative protein kinase related to the Raf family of SerlThr kinases.