In line with Toll-6’s tumor-promoting function in QykiACT/scrib−/− tumors, clonal overexpression of an activated form of Toll-6 (Toll-6ACT) in the E-A disc was sufficient to synergize with QykiACT, ykiS168A, or ykiS111A.S168A.S250A (yki3SA) to induce malignancy, as characterized by increased tumor volume, enhanced invasive migration toward VNC, decreased pupation rate, and formation of Mmp1+ protrusions toward the VNC (Figs. 2A–E and EV2A–F). The gene discussed is MMP1; the disease is neoplasm.