The disruption of the MyD88-ROR-γt regulatory axis by dysbiosis in food allergy organisms led to decreased IgA and increased IgE responses to the gut microbiota, which were reproduced upon Treg cell-specific deletion of Rorc. Abdel-Gadir et al. [54] (2019) suggested that an anti-microbiota Th2 response may be elicited during hypersensitive immune response to foods and may play a critical role in disease initiation, persistence, and outcome [54]. The gene discussed is RORC; the disease is food allergy.