This issue is complicated by EBP’s unique multi-drug binding capacity and the possibility that EBP lowers the intracellular concentration of drugs that inhibit its activity [83,110,111], which provide an alternative explanation for the findings in which the knockdown of EBP conferred the tumor cell’s sensitivity (and vice versa) to its inhibitors (such as clemastine and CW3388). This evidence concerns the gene EBP and neoplasm.