Through these investigation of mechanism in docetaxel-resistant gastric cancers, we can conclude that therapies aimed at reducing FOXM1 or its down-stream target Stathmin will serve as a method of sensitizing tumour cells to docetaxel therapies, and with the addition of a FOXM1 or Stathmin inhibitor to a chemotherapeutic regimen, the drug effective doses would be lower and the side effects for patients could be potentially reduced. This evidence concerns the gene STMN1 and neoplasm.