While all three GFP-LIMK1 fusions resulted in an increased and equivalent invasive phenotype (Figure 6), which correlated with cofilin, FAK, Src, AKT, and Erk phosphorylation (Figures 3 &4), the tumor growth response of the different GFP-LIMK1 fusions did not strictly correlate with their cofilin-FAK signaling activity (Figure 7). The gene discussed is PTK2; the disease is neoplasm.