Our co-IP and PLA results provide clear evidence for a GD2/c-Met association, and are consistent with observations by P. Delannoy's group that GD2 is involved in c-Met activation and subsequent activation of MEK/Erk and PI3K/Akt signaling pathways, leading to enhanced breast cancer cell migration and proliferation [15, 16]. The gene discussed is AKT1; the disease is breast carcinoma.