A clinical case with a chromosomal breakpoint upstream of the IGF-II gene, separating the gene from some of its telomeric enhancers, has been reported to result in intra-uterine growth retardation (consistent with the recognised role of IGF-II in fetal development) but also resulted in the development of atypical early type 2 diabetes that was associated with insulin resistance and a marked increase in abdominal adiposity [111]. This evidence concerns the gene IGF2 and Insulin resistance.