we examined the consequence of Aurka chemical on the weight of V617F/EpoR cells to CDDP. Apparently, Aurka chemical somewhat paid down the viability of V617F/EpoR cells and dramatically improved the sensitivity of V617F/EpoR cells to CDDP. Furthermore, Aurka inhibitor enhanced the expression of p53 in cells. This statement well fits the effect shown in Fig. 4 and emphasizes that kinase activity of Aurka is important for the regulation of p53 stability. Furthermore, both activation of caspase 3 and DNA fragmentation were somewhat detected in cells treated with Aurka inhibitor, and therapy with Aurka inhibitor considerably increased CDDP induced apoptosis in V617F/EpoR cells. Taken natural angiogenesis inhibitors together, it’s recommended that Aurka is critical for resistance to DNA damage in cells transformed by JAK2 V617F mutant and that Aurka chemical is an effective drug for MPNs. In the present research, we discovered Aurka as an essential gene caused by JAK2 V617F mutant and responded that the expression of Aurka is governed by c Myc. Our results confirmed that the expression of c Myc is also upregulated by JAK2 V617F mutant, though it remains to be clarified how a expression of c Myc is caused by JAK2 V617F mutant. As shown in Fig. 3A, JAK2 V617F mutant triggers resistance to CDDP treatment, and this is specifically eliminated by the knock-down of endogenous Aurka and by inhibition of Aurka employing a specific chemical, suggesting that Aurka could possibly be essential for the resistance Organism to CDDP treatment induced by JAK2 V617F. Apparently, the expression degree of p53 was down regulated by overexpression of Aurka and up regulated by knockdown of Aurka. Formerly, in-vitro studies have shown that Aurka phosphorylates p53 at Ser315, leading to its ubiquitination by proteolysis and Mdm2. In addition they confirmed that silencing of Aurka leads to less phosphorylation of p53 at Ser315 and enhances the stability of p53. In the present study, we observed that the expression level of p53 was increased when Aurka KD mutant was Decitabine molecular weight expressed or endogenous Aurka was inhibited by its specific inhibitor, showing that kinase activity of Aurka clearly contributes to the instability of p53 downstream of JAK2 V617F mutant. When contemplating these results, it’s believed that Aurka KD mutant functions as a negative mutant in p53 expression, even though the system by which Aurka KD mutant prevents the downregulation of p53 expression has not been elucidated in this study. Moreover, Mao et al. Noted the status of p53 locus affected the function of Aurka by utilizing p53 deficient mice. These studies strongly support a substantial relationship between Aurka and p53, therefore, in considering treatment for MPNs, not only examining the pres-ence of JAK2 V617F mutation in patients but also examining the position of their p53 locus will become important in the future.