Collectively, these findings underscore that hyperglycemia differentially impacts metabolic programming in Tregs and Tconvs, leading to altered expression of key immune checkpoints, such as TIGIT and CTLA-4, as well as other molecules that support Tregs’ functionality, such as CD39, or the expression of chemokines (CCR5 and CXCR4). The gene discussed is CXCR4; the disease is Hyperglycemia.