However, these authors also show, in a T1DM preclinical model, that the dysregulation in the gut microbiome is important in driving a ‘bystander’ enhancement of effector function in CD8+ T cells [44], indicating that variations in the gut microbiome are an integral aspect of the strength of ‘autoimmune’ responses, with relevance to initial symptom severity [44]. This evidence concerns the gene CD8A and type 1 diabetes mellitus.