Contextually, IL-17A levels in γδ T cells may be directly modulated by the gut microbiota and dietary factors, reflecting their responsiveness in local microenvironments (164), while IL-17 production by Th17 cells relies on more complex regulatory mechanisms, including extracellular signals (e.g., IL-23 activation), transcription factors (e.g., RORγt), RNA, and epigenetic modifications, all of which influence their differentiation and function in the stroke microenvironment (165, 169, 170). This evidence concerns the gene IL17A and Stroke.