Inflammatory Bowel Disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a complex and multifactorial disorder characterized by chronic inflammation of the gastrointestinal tract. While the etiology of IBD remains incompletely understood, genetic factors play a significant role in disease susceptibility, severity, and response to therapies. This review aims to summarize current knowledge on genetic polymorphisms associated with IBD, focusing on their implications for disease susceptibility, severity, and response to therapies. Genome-wide association studies (GWAS) have identified numerous genetic variants contributing to the risk of developing CD and UC. NOD2 variants are strongly associated with CD susceptibility, while variants in genes such as IL23R are associated with UC susceptibility. Moreover, recent studies have highlighted shared genetic risk factors between CD and UC, underscoring the overlapping pathogenesis of these disorders. In addition to disease susceptibility, genetic polymorphisms have been implicated in disease severity and progression. Variants in genes related to the innate and adaptive immune responses, such as ATG16L1 and IL10, have been associated with more severe disease phenotypes in both CD and UC patients. Understanding the genetic basis of disease severity may aid in identifying high-risk patients who require more aggressive treatment strategies. Furthermore, genetic factors influence the response to IBD therapies, including conventional immunosuppressive agents and biologic agents targeting specific cytokines.