Improvement of complex I and IV activity, redox status and membrane potential after intranasal insulin administration in STZ-induced early type 2 diabetic mice was associated with an increase in the activity of the mitochondrial ATP-sensitive large conductance Ca2+-activated potassium channel (mitoBKCa) along with upregulation of the expression of its β2 subunit [38]. The gene discussed is INS; the disease is type 2 diabetes mellitus.