HOTAIR knockdown inhibited cell growth and invasion while enhancing cell death by increasing the expression of miR-34a, which in turn led to the activation of the AKT and Wnt/β-catenin signalling pathways in Taxol-resistance HCC cell lines (Duan et al., 2020); 6) in pancreatic cancer, Wang et al. suggested that HOTAIR overexpression is inducted by gemcitabine treatment in pancreatic CSCs triggering acquired resistance. The gene discussed is HOTAIR; the disease is hepatocellular carcinoma.