Functional dyspepsia （FD） is a constellation of functionalupper abdominal complaints with poorly elucidatedpathophysiology. However, there is increasing evidencethat susceptibility to FD is influenced by hereditaryfactors. Genetic association studies in FD have examinedgenotypes related to gastrointestinal motilityor sensation, as well as those related to inflammationor immune response. G-protein b3 subunit genepolymorphisms were first reported as being associatedwith FD. Thereafter, several gene polymorphisms includingserotonin transporter promoter, interlukin-17F,migration inhibitory factor, cholecystocynine-1 intron1, cyclooxygenase-1, catechol-o-methyltransferase,transient receptor potential vanilloid 1 receptor,regulated upon activation normal T cell expressed andsecreted, p22PHOX, Toll like receptor 2, SCN10A, CD14and adrenoreceptors have been investigated in relationto FD; however, the results are contradictory. Severallimitations underscore the value of current studies.Among others, inconsistencies in the definitions of FDand controls, subject composition differences regardingFD subtypes, inadequate samples, geographicaland ethnical differences, as well as unadjustedenvironmental factors. Further well-designed studiesare necessary to determine how targeted genespolymorphisms, influence the clinical manifestations andpotentially the therapeutic response in FD.