Coupled with insulin deficiency and defective suppression of alpha-cell glucagon secretion in the postprandial period (due to the loss of paracrine inhibition by insulin secreted from the neighboring beta cells) [169,170], amylin deficiency represents an additional cause of poor postprandial glucose control, postprandial hyperglucagonemia and increased glycemic variability in patients with T1D [168]. The gene discussed is INS; the disease is type 1 diabetes mellitus.