These abnormalities may be caused by a heterogeneity of ABA-related dysfunctions occurring in T2D, such as resistance to the effect of ABA (inducing an increase of ABAp, as occurs with insulin in insulin-resistant subjects), or the inability of ABAp to increase in response to hyperglycemia (causing ABAp levels to be in the normal range despite hyperglycemia). The gene discussed is INS; the disease is type 2 diabetes mellitus.