Consequently, podocytes in a diabetic environment can release TNF-α and MCP-1, which promote macrophage migration and induce the expression of T-cell immunoglobulin and mucin domain-3 (TIM-3) on renal macrophages through the NF-κB/TNF-α pathway, thereby contributing to aggravate podocyte injury in diabetic kidney disease and exacerbating the progression of diabetic nephropathy [43]. Here, HAVCR2 is linked to diabetic kidney disease.