MiR-27a inhibits the expression of the Sp repressor ZBTB10/RINZF [15], leading to the overexpression of Sp factors and, as a consequence, to the increase of Sp-dependent antiapoptotic and angiogenic molecules’ number, e.g. survivin and vascular endothelial growth factor (VEGF), responsible for cancer development [16]. This evidence concerns the gene VEGFA and cancer.