Together with insulin, ABAp is also undetectable or very low in type 1 diabetes (T1D) patients, suggesting that β-cells are the principal source of endogenous ABA in humans; thus, the demise of β-cells in T1D greatly reduces the availability of both hormones regulating glycemia, only one of which is currently replaced by therapy. The gene discussed is INS; the disease is type 1 diabetes mellitus.