It has been suggested that pharmacologic resistance in GBM is due to a high concentration of antiapoptotic proteins (Bcl-2, Bcl-xL and Mcl-1) and a low expression of proapoptotic proteins (BAX, Bak, pBad, pBim, and Survivin), favoring the switching-on of oncogenes and genetic instability that promote tumor survival and resistance to radiotherapy, chemotherapy, and immunotherapy. The gene discussed is BCL2; the disease is neoplasm.