Considering that human ANLN is normally degraded after a mitotic exit and sequestered in the nucleus during interphase, its overexpression may overwhelm these normal regulatory mechanisms, freeing ANLN to have an impact on the actin–myosin cytoskeleton during the events besides cytokinesis, including, for example, cell motility, and thus it directly contributes to cancer progression. The gene discussed is ANLN; the disease is cancer.