Additionally, the biophysical and biochemical alterations of predominantly CaV3.2 subtype, such as T-current increase and T-channel mRNA expression, accompanied the development of painful PDN and hyperglycemia, indicating that metabolic changes leading to hyperglycemia are affecting DRG T-current in a similar causative fashion in both type I and II painful PDN, leading to the hyperexcitability of peripheral sensory neurons underlying hyperalgesia and allodynia. The gene discussed is CACNA1H; the disease is Hyperglycemia.