“Metabolic memory” refers to the phenomenon in which early episodes of hyperglycemia leave lasting molecular imprints—such as epigenetic modifications and persistent activation of signaling pathways (e.g., PKC, NF-κB, and transforming growth factor (TGF)-β)—that drive the progression of diabetic complications even after glycemic control is achieved.72 In DKD, prior high-glucose exposure “primes” kidney cells for persistent injury so that inflammation and fibrosis continue despite later glycemic control. The gene discussed is PRRT2; the disease is Hyperglycemia.