From these first two observations, it can be concluded that CX-2009 is capable of targeting CD166-expressing tumors when compared with its parental derivatives, indicating that proteolytic activation of CX-2009 inside the tumor, which is required to allow CD166 binding, does not limit tumor targeting, thus supporting the equal therapeutic efficacy of CX-2009 and CX-1031 as demonstrated in the same tumor model (Figure 8). This evidence concerns the gene ALCAM and neoplasm.