We　reported　two　Au　clusters　with　precisely　controlled　molecular　size　(Au(5)Peptide(3)　and　Au(22)Peptide(10))　showing　different　antitumor　effects.　In　vitro,　both　Au(5)Peptide(3)　and　Au(22)Peptide(10)　were　well　taken　up　by　human　nasopharyngeal　cancer　cells　(CNE1　cells).　However,　only　Au(5)Peptide(3)　significantly　induced　CNE1　cell　apoptosis.　Further　studies　showed　that　CNE1　cells　took　up　Au(5)Peptide(3)　(1.98　X　10(-15)　mol/cell),　and　9%　of　them　entered　mitochondria　(0.186　X　10(-15)　mol/cell).　As　a　comparison,　the　uptake　of　Au(22)peptide(10)　was　only　half　the　amount　of　Au(5)Peptide(3)　(1.11　X　10(-15)　mol/cell),　and　only　1%　of　them　entered　mitochondria　(0.016　X　10(-15)　mol/cell).　That　gave　11.6-fold　more　Au(5)Peptide(3)　in　mitochondria　of　CNE1　cells　than　Au(22)Peptide(10).　Further　cell　studies　revealed　that　the　antitumor　effect　may　be　due　to　the　enrichment　of　Au(5)Peptide(3)　in　mitochondria.　Au(5)Peptide(3)　slightly　decreased　the　Mcl-1　(antiapoptotic　protein　of　mitochondria)　and　significantly　increased　the　Puma　(pro-apoptotic　protein　of　mitochondria)　expression　level　in　CNE1　cells,　which　resulted　in　mitochondrial　transmembrane　potential　change　and　triggered　the　caspase　9　caspase　3　PARP　pathway　to　induce　CNE1　cell　apoptosis.　In　vivo,　CNE1　tumor　growth　was　significantly　suppressed　by　Au(5)Peptide(3)　in　the　xenograft　model　after　3　weeks　of　intraperitoneal　injection.　The　TUNEL　and　immuno-histochemical　studies　of　tumor　tissue　verified　that　CNE1　cell　apoptosis　was　mainly　via　the　Puma　and　Mcl-1　apoptosis　pathway　in　the　xenograft　model,　which　matched　the　aforementioned　CNE1　cell　studies　in　vitro.　The　discovery　of　Au-5　but　not　Au-22　suppressing　tumor　growth　via　the　mitochondria　target　was　a　breakthrough　in　the　nanomedical　field,　as　this　provided　a　robust　approach　to　turn　on/off　the　nanoparticles＇　medical　properties　via　atomically　controlling　their　sizes.