In contrast, NK-1R antagonists, in a concentration-dependent manner, counteract all the pathophysiological effects of SP in glioma: inhibiting glioma cell proliferation (antimitogenic effect), inducing programmed cell death in glioma cells (apoptosis), counteracting the Warburg effect in glioma cells, decreasing both endothelial cells’ proliferation and angiogenesis, providing anti-inflammatory effects, and preventing invasion and migration (infiltration and metastases) of glioma cells [8,9,11]. The gene discussed is TACR1; the disease is glioma.