These observations, together with the lack of mutation in AURKA, implicated that the cancer cells harboring resistance to alisertib could be dependent on the aberrant amplification and activation of STAT1 rather than acquired mutations in the AURKA gene or induction of IFN products in vivo, which implicated that inhibition of Aurora-A could generally elevate STAT1 expression. The gene discussed is IFNA1; the disease is cancer.