The attenuation of GABA synthesis and secretion in the islets due to β-cell stress and death during diabetes development is expected to reduce GABA's (1) autocrine effects on β-cell replication and survival [3–8], (2) inhibition of glucagon secretion from α-cells [33], and (3) regulatory action on inflammatory infiltrates in the islets [12]. This evidence concerns the gene GCG and diabetes mellitus.