ATG9A　is　a　transmembrane　protein　essential　for　macroautophagy/autophagy　that　drives　autophagosome　formation　by　delivering　essential　proteins　and　lipids　to　the　phagophore　through　vesicle　trafficking.　Here,　we　demonstrate　that　the　atypical　Rho　GTPase　RHOD　is　required　for　ATG9A　trafficking　and　stimulates　autophagosome　formation.　Upon　starvation,　RHOD　interacted　with　ATG9A　and　accompanied　ATG9A　trafficking　from　the　Golgi　toward　phagophores.　In　addition,　starvation-induced　high　levels　of　RHOD　resulted　in　Golgi　fragmentation　to　further　promote　ATG9A　vesicle　export　from　the　trans-Golgi　network　to　the　peripheral　region.　Loss　of　RHOD　suppressed　ATG9A　trafficking　and　reduced　the　distribution　of　ATG9A　on　the　phagophore.　Moreover,　WHAMM　(WASP　homolog　associated　with　actin,　golgi　membranes　and　microtubules)　forms　a　complex　with　RHOD　and　participates　in　this　process　in　a　RHOD-dependent　manner.　Importantly,　RHOD　mutants,　which　lack　the　exon　II-containing　effector　region　motif　that　is　required　for　ATG9A　binding　or　lack　the　CAAX　box　that　is　responsible　for　membrane　targeting,　fail　to　stimulate　ATG9A　trafficking　and　autophagosome　formation.　Furthermore,　RHOD　plays　a　distinct　suppressor　role　in　tumor　development,　partly　associated　with　its　regulatory　effect　on　autophagy.　These　findings　reveal　the　important　roles　of　RHOD　in　autophagy　and　tumor　development.Abbreviation:　ATG9A:　autophagy　related　9A;　BafA1:　bafilomycin　A1;　BiFC:　bimolecular　fluorescence　complementation;　co-IP:　co-immunoprecipitation;　EBSS:　Earle＇s　balanced　salt　solution;　FM:　full　culture　medium;　KO:　knockout;　MAP1LC3/LC3:　microtubule　associated　protein　1　light　chain　3;　PUP-IT:　pupylation-based　interaction　tagging;　RHOD:　ras　homolog　family　member　D;　SQSTM1:　sequestosome　1;　TGN:　trans-Golgi　network;　VC:　Venus　C-terminal;　VN:　Venus　N-terminal;　WHAMM:　WASP　homolog　associated　with　actin,　golgi　membranes　and　microtubules;　WIPI2:　WD　repeat　domain,　phosphoinositide　interacting　2;　WT:　wild-type;　3-MA:　phosphatidylinositol　3-kinase　(PtdIns3K)　inhibitor　3-methyladenine.