Background:Ferroptosis　was　reported　to　possess　the　therapeutic　potentials　in　various　human　cancers.　In　the　present　study,　we　explored　the　expression,　clinical　significance　and　the　molecular　mechanism　of　FK506　binding　protein　3　(FKBP3)　in　the　progression　of　lung　adenocarcinoma　(LUAD).Material　and　Method:Cox　regression　was　performed　to　obtain　the　prognosis　related　to　differentially　expressed　genes　(DEGs)　in　LUAD　datasets　from　TCGA.　We　also　downloaded　the　ferroptosis-related　gene　datasets　from　GeneCards.　Venn　diagram　was　performed　to　find　the　intersecting　genes　and　FKBP3　was　selected　as　the　targeted　gene　by　analyzing　the　diagnostic　and　prognostic　values　of　Top10　intersecting　genes.　Moreover,　univariate　and　multivariate　analyses　were　performed　to　evaluate　the　association　between　clinicopathological　factors　and　survival　rates.　GO/KEGG　and　GSEA　analysis　was　performed　to　explore　the　function　of　FKBP3　in　LUAD　progression.　Protein-protein　interaction　(PPI)　network　was　performed　via　STRING　database　and　the　top10　hub　genes　were　selected.　Finally,　the　relationship　between　FKBP3　and　immune　infiltration　was　explored　by　ssGSEA　analysis.Results:Firstly,　184　genes　associated　with　the　prognosis　of　LUAD　and　ferroptosis　were　obtained.　FKBP3　was　found　to　be　significantly　associated　with　a　poor　overall　survival　rate　of　LUAD　patients.　Immunohistochemical　staining　results　showed　that　FKBP3　was　highly　located　in　cytoplasm　and　membrane　of　cells　in　LUAD　tissues.　PPI　network　analysis　results　showed　that　HDAC1,　YY1,　HDAC2,　MTOR,　PSMA3,　PIN1,　NCL,　C14orf166,　PIN4,　and　LARP6　were　the　top10　hub　genes.　Furthermore,　spearman　analysis　results　showed　that　the　expression　of　FKBP3　was　positively　correlated　with　the　abundance　of　Th2　cells　and　T　helper　cells.Conclusion:High　level　of　FKBP3　was　associated　with　poor　prognostic　outcomes　of　LUAD　patients,　which　also　inhibited　immune　infiltration　in　LUAD　tissues.　Additionally,　FKBP3　was　involved　in　regulating　the　ferroptosis　process　in　LUAD　patients.　Thus,　FKBP3　possessed　the　tumor　promotion　role　might　be　involving　in　regulating　ferroptosis　and　immune　infiltration　in　LUAD　progression.