Remarkably, a subgroup of T1D patients with diabetes‐related macrovascular complications revealed a stronger proinflammatory phenotype characterized by a lower percentage of FOXP3+ Treg, higher proportions of CCR4 expressing CD4 and CD8 T cell subsets, classical, CD196+, and CD194+ monocyte subsets, a lower Treg/conventional T‐cell ratio, an increased proinflammatory cytokine (TNF‐α, IFN‐γ), and a decreased anti‐inflammatory (IL‐10) producing potential compared to T1D patients without macrovascular complications [63]. This evidence concerns the gene TNF and type 1 diabetes mellitus.