In type 2 diabetes mellitus mouse model, KLF5 is induced by high insulin level in the blood, and overexpression of KLF5 significantly inhibits nitric oxide synthase 3 (NOS3) transcription and diminishes the level of endothelial nitric oxide synthase (eNOS), thus compromising EC proliferation and blunting angiogenic response. This evidence concerns the gene INS and diabetes mellitus.