All of the above-mentioned rationales may explain the lower survival rate and worse prognostic outcomes in the MDKhigh group, indicating that MDK plays a central role in GBM biology, and its inhibition might be a feasible strategy to increase the treatment efficacy of larger treatment regimens through inhibition of GBM cell proliferation and EMT as well as rebalancing of the tumor microenvironment. This evidence concerns the gene MDK and neoplasm.