Altogether, the findings in this report highlight an improved structural understanding by which proinsulin misfolding might be attacked pharmacologically, a) to block exposure of unpaired cysteines, and b) to limit the increased aberrant proinsulin–proinsulin associations [49] which are a hallmark of MIDY and perhaps also of type 2 diabetes [32]. The gene discussed is INS; the disease is type 2 diabetes mellitus.