Moreover, we demonstrated that the promotive or suppressive role of uMtCK overexpression or knockdown on the expression of HK2 in GC cells could be apparently counteracted by treatment with JNK-MAPK/JUN signaling pathway inhibitors or activation agent, respectively; however, these processes were abolished when binding site 1 was mutated in GC cells (Fig. 4l, m). This evidence concerns the gene JUN and gastric cancer.