In that context, we previously showed that the ectopic expression of the GD3S in breast cancer cells induced the accumulation of b- and c-series gangliosides at the cell surface together with the acquisition of a proliferative phenotype and enhanced tumor growth [16,17], due to the specific and constitutive activation of c-Met receptor in the absence of ligand, and subsequent activation of the PI3K/Akt and Erk/MAPK pathways in GD2 expressing breast cancer cells [18]. The gene discussed is AKT1; the disease is breast cancer.