To further investigate the potential role of EcR signaling in regulating tumor progression, we overexpressed several well-established downstream target genes of EcR in the scrib−/−, wts−/− tumors, including Hr3, ftz-f1, Eip93F, br, and E75. Surprisingly, we observed that only the overexpression of E75 significantly enhanced the overgrowth of scrib−/−,wts−/− tumors, while the expression of other genes impeded tumorigenesis (Fig. 1H,H’). This evidence concerns the gene SCRIB and neoplasm.