APOD and Hypoglycemia: Our results also confirmed the previously reported overexpression of several genes in SFTs as compared with STSs, such as BCL2[10], and 10 out of the 16 discriminating genes quoted in the core text of Hajdu’s report [22]: ALDH1A1, APOD, COL16A1, COL17A1, COL6A3, DDR1, ERBB2, FGFR1, GRIA2, and IGF1. We also confirmed the strong overexpression of IGF2, responsible for hypoglycemia observed in the Doege-Potter syndrome and related to loss of imprinting (LOI) [22] by aberrant methylation.