Selective LFDI-mediated antagonism of ObR abrogates NOTCH signaling, suggesting a critical role of leptin/ObR in the modulation of NOTCH-dependent growth, proliferation and migration of glioblastoma cells [24], and a previous study suggested that this invasiveness and migration were driven by increased levels of matrix metalloproteinase (MMP)-13 via the MAPK pathway (Figure 1) [25]. The gene discussed is LEPR; the disease is glioblastoma.