Since DYRK1B can promote cell cycle arrest and differentiation [22, 24, 25, 45, 55, 56], such loss-of-function mutations suggest that any oncogenic properties of DYRK1B are, at best, context-dependent; indeed, they may even suggest tumour suppressor functions for wild-type DYRK1B. Here, DYRK1B is linked to neoplasm.