Norovirus is a highly contagious virus that causes gastroenteritis, an inflammation of the stomach and intestines. It is one of the most common causes of foodborne illness in the United States, with over 20 million cases reported each year. While norovirus infections can be mild and self-limiting, they can also cause severe dehydration and even death in some cases. Recent research has identified a gene called FUT2 (fucosyltransferase 2) as being associated with increased susceptibility to norovirus infection. FUT2 is a glycosyltransferase enzyme involved in the synthesis of fucose sugars on cell surfaces. These sugars are important for many biological processes including immune system function, cell adhesion, and viral entry into cells. In humans, FUT2 exists in two forms: secretor (Se) or non-secretor (see). Individuals who are Se have functional copies of both alleles while those who are se only have one functional allele resulting in reduced activity levels of this enzyme. Studies have shown that individuals who lack functional copies of FUT2 (i.e., those who are se/se) are more susceptible to norovirus infection than those with at least one functioning copy (Se/se or Se/Se). This increased susceptibility appears to be due to differences in how these individuals interact with the virus itself; specifically, it appears that viruses bind more readily to cells lacking fucose sugars which may explain why people without functional copies of FUT2 seem more prone to infection by certain strains of norovirus such as GII4P[6]. In addition to its role in increasing susceptibility to norovirus infections, recent studies suggest that variations within the FUT2 gene may also influence other aspects related to gastrointestinal health such as inflammatory bowel disease risk and gut microbiome composition. For example, some studies have found associations between specific variants within this gene and higher rates of Crohn’s disease while others suggest links between certain variants and altered microbial communities within the gut microbiota which could potentially lead to changes in overall health status over time if left unchecked. Overall, research into how genetic variation affects our response towards infectious agents like noroviruses continues apace but much remains unknown about exactly how different genes contribute towards our individual susceptibilities towards various pathogens – including ones like NoroViruses - so further work will need to be done before we fully understand all their implications for human health.