Previously, DYRK2 was primarily considered as a cancer suppressor, which can promote phosphorylation of P53 to induce apoptosis20,21, facilitate degradation of c-JUN and c-MYC to inhibit the transition of the cell cycle from G1 to S phase22,23, and accelerate the degradation of snail to suppress epithelial-to-mesenchymal transition (EMT) and cell migration and so on24,25. The gene discussed is JUN; the disease is cancer.