The focus of our research is calcium signaling and its relationship with autophagy in cancer. We study how ion channels partipate in glioblastoma progression. So far we have shown that silencing of voltage-gated T-type Ca 2+ channels (Cav3 channels) deregulates the endoplasmic reticulum unfolded protein response and autophagy processes in GBM cell lines and primary cultures, leading to GBM cell death or to a proliferative arrest. Furthemore, we have reported that Cav3 pharmacological blockers of the tetralol family disrupt autophagy and cause GBM cell death by actions other than channel block. Our overall efforts are directed to find new targets to disrupt homeostastic cell processes in normoxic and hypoxic tumor environments.