Combined siRNA knockdown of both EPH-A2 and EPH-B2 genes, herein, shown and known [18] to be overexpressed in ERMS tumours, replicated many of the phenotypic effects observed in ERMS cells after drug exposure, confirming that GLPG1790 activity is mediated by the efficient impairment of EPH activity [21]. This evidence concerns the gene EPHB2 and neoplasm.