Our findings suggest that a very low dose of SU in T2DM achieves a similar partial closure of the KATP channels as seen for high dose SU in NDM, working primarily to prime the beta-cell to other secretagogues such as the incretins or amino acids, resulting in glucose regulated insulin secretion and no insulin secretion in the presence of normal or low blood glucose. This evidence concerns the gene INS and type 2 diabetes mellitus.