In addition, the depletion or inhibition of DYRK1B enhances the DNA damage, apoptosis and sensitivity to reactive oxygen species (ROS) or chemotherapeutic drugs targeting proliferating cells [15,104,121,122,123], as well as the sensitivity to compounds that target pathways favoring proliferation in cell lines of different tumor origins, such as mTOR and MEK inhibitors [107,109] (Figure 2). This evidence concerns the gene DYRK1B and neoplasm.