Overall, combining EGFR targeted therapy with HDAC inhibition reduces the development of resistance in glioblastoma cells in vitro by preventing compensatory overexpression of wild-type EGFR/EGFRvIII and represses wtEGFR/EGFRvIII in cells that have attained resistance to targeted therapy by increased expression of these oncogenes, thereby resensitizing the cells to targeted therapy. This evidence concerns the gene EGFR and glioblastoma.