Our data confirmed that Axl was a crucial target in the inhibition of GBM EMT-related genes, including N-cadherin, Twist, Snail, and Slug expression; the controlled-release BP wafer not only delivered a significant drug concentration but also extended the drug diffusion distance within the tumor cells, which in turn significantly increased the survival rate of the treated animals and reduced tumor invasion and migration through a decrease of Axl expression in the in vitro and in vivo xenograft animal models (Figure 1) [80]. This evidence concerns the gene AXL and neoplasm.