Inoculation with endophytic fungus Gilmaniella sp. induced multiple responses in host plantlets of Atractylodes lancea, including the burst of NO, SA, H 2 O 2 , and the accumulation of volatile oil. To investigate the pathways that the three signal molecules affect the volatile oil production, the plantlets were treated with NO specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO), SA synthesis inhibitor trans-cinnamic acid (trans-CA), membrane NADPH oxidase inhibitor diphenylene iodonium (DPI) and catalase (CAT). The results showed pretreatment of plantlets with cPTIO, DPI/CAT and trans-CA inhibited the burst of signal molecules and volatile oil accumulation induced by the fungus. Exogenous NO donor SNP could promote SA and H 2 O 2 production as well as volatile oil accumulation. Combined application of trans-CA and DPI/CAT could inhibit the promotion effects of exogenous NO. Exogenous SA and H 2 O 2 had no effects on NO production, but they could reverse the total inhibitory effects of cPTIO, CAT/DPI and trans-CA toward volatile oil accumulation. Exogenous H 2 O 2 had promotion effect on SA production, yet CAT/DPI could not significantly prevent SA synthesis. These data indicated NO mediates violate oil accumulation induced by the fungus through SA and H 2 O 2 dependent pathways. H 2 O 2 can regulate SA production, but does not act as upstream signal molecule.