Since the MaxiK α‐subunit expression is low with diabetes, and this is not reversed with insulin treatment, the proposed use of pharmacologic MaxiK channel openers would either have to be used at much higher doses than when used in non‐diabetics to obtain the same physiological effect, or, the level of target is so low, that attempts to increase activity through the use of pharmacologic agents would have no effect on physiology. The gene discussed is KCNMA1; the disease is diabetes mellitus.