These factors form a complex to activate the P53 promoter,33, 34 which is an important observation because P53‐dependent apoptosis is the major route by which DNA damaging chemotherapy drugs induce cellular apoptosis.33 The combined use of JAK2 and HSP90 inhibitors resulted in improved efficacy in drug‐resistant chronic leukemia,35 and inhibiting JAK2 activity can reverse paclitaxel resistance in human ovarian cancer cells.36 Our results are consistent with these reports. This evidence concerns the gene JAK2 and ovarian carcinoma.