As a result, not only do we demonstrate that microtubules in FOXM1-overexpressed cell lines fail to polymerize in response to docetaxol treatment but also that FOXM1 directly targeted and up-regulated the microtubule-destabilizing protein Stathmin rather than MCAK, which also correlated with docetaxel resistance in gastric cancer cells, indicating that FOXM1 could bound at the Stathmin gene promoter and prevented the tubulin polymerization to induce docetaxel resistance in gastric cancers. Here, FOXM1 is linked to gastric cancer.