Glioblastoma multiforme is a dismal disease with a prognosis of 12-14 months following diagnosis. Patients diagnosed with this disease have a 5% 5-year survival rate. Unfortunately, these statistics have not changed in 30 years despite ongoing research within the field. The current standard of care therapy of gross total resection (if eligible) followed by radiation and chemotherapy, temozolomide, is limited and only offer a few months of prolonged life. Genomic analysis of tumors has identified many mutations, amplifications, and genetic anomalies within the cancer DNA repertoire. Improving our understanding of the molecular alterations in this disease through these identifications provide us with the potential ability to target proteins specifically aiding to the survival of cancer. Some of these mutations have been targeted successfully and have prolonged life in other cancers, e.g.CML and lung cancer. However, clinical trials have revealed that certain targeted therapies, such as avastin and cetuximab, do not prolong life in glioblastoma. Glioblastoma is known for its highly mutated DNA, its highly migratory phenotype, and its high heterogeneity, making this tumor difficult to target. One goal is to find an essential oncoprotein that the tumor is addicted to, a theory known as oncogene addiction, to target and eliminate the cells upon inactivation of the oncogene. Another is to find a protein that is only expressed by the tumor cell, known as a tumor specific antigen, to reduce toxicity levels of therapy. Unfortunately, these tasks are not as easily accomplished as they were originally theorized. MERTK, a receptor tyrosine kinase, is a protein that is essential in glioblastoma with regard to signaling for cellular migration, pro-survival and pro-proliferative signaling pathways. Targeting MERTK is promising because it is aberrantly expressed in 90% of glioblastoma patient samples tested. However, taking into consideration the failed clinical trials for monotherapy against EGFR, another receptor tyrosine kinase targeted in GBM, combination therapy may provide a better approach in the treatment of GBM. Two approaches were tested. One approach combined therapy of MERTK inhibition with either chemotherapy or autophagy manipulation. The second approach is to stimulate the immune system alongside EGFR inhibition, with the hope of enabling a greater response in patients.