Functional gastrointestinal disorders (FGIDs) are increasingly recognized as arising from specific underlying mechanisms, presenting significant opportunities for personalized medicine approaches. In patients experiencing functional upper gastrointestinal symptoms (UGI symptoms), a notable proportion—around 25%—have distinct conditions: delayed gastric emptying, reduced gastric accommodation, both impairments, or normal function, potentially linked to increased sensitivity in the gastric or duodenal regions. Treatment strategies targeting these mechanisms may include prokinetics, gastric relaxants, and central neuromodulators. For those with functional lower gastrointestinal symptoms, particularly diarrhea or constipation, similar mechanistic patterns are observed. Over 30% of patients with functional constipation may have pelvic floor dyssynergia, while 5% exhibit colonic inertia due to neural or interstitial cell loss in the myenteric plexus. Additionally, 25% of individuals with diarrhea-predominant irritable bowel syndrome (IBS-D) may experience bile acid diarrhea, with variations in disaccharidase deficiencies influenced by ethnicity. In patients presenting with predominant pain or bloating, the impact of fermentable carbohydrates should be considered. The application of personalized medicine is further advanced through pharmacogenomic insights, particularly regarding key drug metabolism genes such as CYP2D6, 2C19, and 3A4, which inform treatment options for FGIDs. While single genetic mutations are rare, ongoing research into mucosal gene expression, especially in IBS-D, is vital. In summary, the time for personalized medicine in the management of FGIDs is upon us, driven by thorough phenotyping and pharmacogenomic insights. However, the precise role of genetic factors in FGID management remains an area for further investigation.