Different molecular characteristics of ACC could be considered potential therapy targets, including overexpression of vascular endothelial growth factors and receptors (VEGF/VEGFR) and insulin-like growth factors and receptors (IGF/IGFR) [3, 4]; PI3K/AKT/mTOR pathway activation as a mediator of VEGF and IGF [5]; high levels of multidrug resistant protein 1 (MDR-1) [6]; gain of chromosomal region 9q34 [7] and the involvement of ABL oncogene and downregulation of bone morphogenetic proteins 2 and 5 (BMPs) [8]. This evidence concerns the gene IGF1 and adrenal cortex carcinoma.