Given that the pharmacological inhibition of MEK1 by PD98059 effectively suppressed the mitogenic activity of leptin [56] and increased the adhesiveness of glioblastoma cells to ECM [57], the ability of SM to directly interact with the components of the SOS/MEK1/ERK2 signaling axis could explain its modulatory effect on the aggressiveness of leptin-induced neuroblastoma cells. The gene discussed is LEP; the disease is glioblastoma.