Shen　et　al.　propose　a　mechanism　for　the　metastasis　of　hepatocellular　carcinoma　(HCC)　cells　through　the　localization　and　translation　modulation　of　the　STAT3　oncogene　by　fragile　X　mental　retardation　protein　(FMRP).　To　this　end,　the　authors　also　find　that　FMRP　knockdown　efficiently　suppresses　HCC　metastasis　in　vitro　and　in　vivo.　Most　hepatocellular　carcinoma　(HCC)-associated　mortalities　are　related　to　the　metastasis　of　cancer　cells.　The　localization　of　mRNAs　and　their　products　to　cell　protrusions　has　been　reported　to　play　a　crucial　role　in　the　metastasis.　Our　previous　findings　demonstrated　that　STAT3　mRNA　accumulated　in　the　protrusions　of　metastatic　HCC　cells.　However,　the　underlying　mechanism　and　functional　significance　of　this　localization　of　STAT3　mRNA　has　remained　unexplored.　Here　we　show　that　fragile　X　mental　retardation　protein　(FMRP)　modulates　the　localization　and　translation　of　STAT3　mRNA,　accelerating　HCC　metastasis.　The　results　of　molecular　analyses　reveal　that　the　3　＇　UTR　of　STAT3　mRNA　is　responsible　for　the　localization　of　STAT3　mRNA　to　cell　protrusions.　FMRP　is　able　to　interact　with　the　3　＇　UTR　of　STAT3　mRNA　and　facilitates　its　localization　to　protrusions.　Importantly,　FMRP　could　promote　the　IL-6-mediated　translation　of　STAT3,　and　serine　114　of　FMRP　is　identified　as　a　potential　phosphorylation　site　required　for　IL-6-mediated　STAT3　translation.　Furthermore,　FMRP　is　highly　expressed　in　HCC　tissues　and　FMRP　knockdown　efficiently　suppresses　HCC　metastasis　in　vitro　and　in　vivo.　Collectively,　our　findings　provide　further　insights　into　the　mechanism　of　HCC　metastasis　associated　with　the　regulation　of　STAT3　mRNA　localization　and　translation.