Promotes the exchange of Ras-bound GDP by GTP (By similarity). May regulate signaling pathways downstream of receptor tyrosine kinase, egl-15 and let-23 (PubMed:10880441). Required for larval and male spicule development, fluid homeostasis, vulva induction, spermatogenesis, and oogenesis by promoting meiosis prophase exit during oocyte maturation (PubMed:10880441, PubMed:17339331). Required for the delamination of G1 cell by promoting the loss of cell junctions and detachment from the excretory system during larval development (PubMed:25371363). Plays a role in nicotinic acetylcholine receptor (nAChR)-mediated sensitivity to nicotine (PubMed:15990870). Regulates synaptic levels of nAchR subunit lev-1 in the nerve cord (PubMed:15990870). Interacts with cmd-1 in the presence of Ca(2+). The DH (DBL-homology) domain may inhibit the Ras-GEF domain, thereby preventing excessive let-60/Ras activation. RNAi-mediated knockdown results in 8% early larval lethality of the progeny. Surviving animals display slow growth, thin body morphology and both spermatogenesis and oogenesis are arrested at the pachytene stage of meiosis I. In addition, males have short and crumpled spicules. RNAi-mediated knockdown prevents multi-vulva induction in let60 n1046, let-23 sa62 or lin-15 n765 mutants and fluid accumulation in clr-1 e1745ts mutant.