Furthermore, the prevalence of insulin therapy among T2D despite low disease duration implicating early beta cell failure as well as the occurrence of ketosis-prone T2D diabetes, which contrasted with the usual obese male phenotype, indicates overlaps with entities such as “thin fat” phenotypes, double diabetes, as highlighted in other countries in the region bearing evidence towards the enigmatic pathophysiology of YOD [27–29]. The gene discussed is INS; the disease is diabetes mellitus.