Pharmacologic inhibition of the kinase Mirk/Dyrk1B by the small molecule inhibitor RO5454948 enabled escape from arrest in G0 quiescence, and increased ROS levels, DNA damage, and apoptosis in pancreatic cancer cells that had entered cycle [10], and escape from quiescence led to more apoptosis in cancer cells with mutant p53 in addition to low expression of G1 CDK inhibitors [11]. This evidence concerns the gene DYRK1B and pancreatic neoplasm.