Given the importance of BTNL8 in regulating the severity of Crohn’s disease (Dart et al., 2023), and given animal models in which γδT cell deficiencies have been associated with disease severity rather than disease incidence, it would be of interest to further investigate the role of this pathway in pediatric IBD and other pediatric inflammatory disorders such as KD where tissue repair may be an essential limit on symptoms. This evidence concerns the gene BTNL8 and inflammatory bowel disease.