These metabolic findings resemble investigations in human Simpson-Golabi-Behmel syndrome adipocytes (62) (in which IFNγ decreased insulin-mediated glucose uptake, also reversed by a JAK1 inhibitor), 3T3-L1 adipocytes34, and primary adipocytes from obese individuals35, but extend these findings. This evidence concerns the gene IFNG and Simpson-Golabi-Behmel syndrome.