In vivo studies [20, 34] demonstrated that the Notch3 activation in podocytes (via infection with adenovirus expressing a constitutively active Notch3 intracellular domain) led to alterations in cell shape (elongation), acquisition of a migratory phenotype, downregulated transcription of p21 and p27 (which promote cell cycle progression), and upregulation of Aurora Kinase B. Unfortunately, aberrantly expressed Aurora Kinase B could induce cell cycle progression but could not support the assembly of a functional mitotic spindle, which induced cell death by mitotic catastrophe. The gene discussed is NOTCH3; the disease is infection.