Furthermore, this study discovered candidate mediators (TGFBR2, CRIM1, TXNIP, DPYSL2, and CRMP1) that may impart treatment resistance following HOXA11 suppression.33 As a conclusion, these results indicate that HOXA11‐AS plays a key role in GBM and it can be a novel therapeutic target for the treatment of GBM. This evidence concerns the gene DPYSL2 and glioblastoma.