Subsequent experiments showed that primary subcutaneous adipocytes and preadipocyte Simpson-Golabi-Behmel syndrome (SGBS) cells, a preadipocyte model, increased T production from 4-androstene-3,17-dione (4AD) when stimulated with insulin, and this was mediated by induction of aldo-keto reductase family 1 member C3 (AKR1C3) [13, 14]. This evidence concerns the gene AKR1C3 and Simpson-Golabi-Behmel syndrome.