Xu and colleagues reported that lncRNA HIF1A-AS1 binds to AKT, enhances AKT/YB1 interaction, and facilitates the phosphorylation of YB1 (pYB1), which is then recruited to the HIF1α promoter to activate its transcription and drive the glycolysis-dependent drug resistance in pancreatic cancer (Fig. 6A) [82]. This evidence concerns the gene HIF1A and pancreatic neoplasm.