Fukuda et al. (2019) showed that pretreatment with the HDAC inhibitor quisinostat downregulates the expression of miR-200c, leading to higher expression of ZEB1 and promoting tumor cell sensitivity to crizotinib. Stockhammer et al. (2020) found that the highly resistant PF240-PE tumor cells to crizotinib and alectinib became sensitive to these ALK inhibitors after treatment with vorinostat. The gene discussed is HDAC9; the disease is neoplasm.