The current research investigated that downregulation of FTO played key roles in suppressing keratinocyte autophagy under both acute and chronic hyperglycemia environments, implying that FTO can be used as a biomarker and potential therapeutic target for diabetic wounds, and modulated m6A modification in TRIB3 mRNA levels via an m6A-YTHDF2-dependent manner. The gene discussed is YTHDF2; the disease is Hyperglycemia.