This adverse effect is evident in DT1 patients, who in the absence of insulin replacement are in a catabolic state that results in severe depletion of both energy stores and protein mass (denutrition and cachexia); eventually, untreated DT1 patients develop severe neuropathy, myopathy, and/or cardiomyopathy due to muscle wasting (D'Souza, Al‐Sajee, & Hawke, 2013). The gene discussed is INS; the disease is Cachexia.