Myc was then shown to mediate increases in aurora kinases A and B. Elevation of AURKA, AURKB, and MYC was confirmed in primary LGLL patient samples, and Myc knockdown in mouse LGL cells showed reduced AurkA and AurkB. The increased aurora kinases led to centrosome aberrations and result in chromosomal aneuploidy, which is a consistent finding in patient LGLL cells. The gene discussed is AURKB; the disease is T-cell large granular lymphocyte leukemia.