Although SU6656 has previously been proven to induce differentiation of megakaryocytic progenitors and trigger polyploidy in primary bone marrow cells, leukemic cell lines and human B lymphocytes, these studies don’t further examine the molecular mechanisms evoking the functional and phenotypic effects caused by SU6656. In contrast, it has been recognized that the effects are as a result of SFK inhibition. However, contact with yet another SFK inhibitor PP2 did not induce similar reactions in any one of our cell systems. For that reason we looked in-the literature biomedical library for similar mobile effects induced by other kinase inhibitors. Curiously, we came across research in which early prometaphase inhibition of Aurora B kinase, which is implicated in a number of crucial events in mitosis, triggered an identical temporary charge during which cells rounded up to undergo mitosis, but left M phase and flattened onto the substratum with polyploid interphase nuclei. We then searched literature sources, i. Elizabeth. Medline/ PubMed and PubChem, for hits on Aurora and SU6656 but these searches made no hits. Coincidently, however, we came across a recently available chemical review by Bain and co workers indicating unselective activities of various kinase inhibitors, including SU6656, Chromoblastomycosis which was shown to be a lot more powerful against Aurora B and C kinase than Lck and Src. To verify that Aurora kinase inhibition causes a similar phenotypic result as SU6656 we exposed cells towards the very specific smallmolecule Aurora kinase inhibitors SNS314 for 72 h. As shown in Fig. 4A all cell lines mentioned above displayed similar morphological characteristics in reaction to SNS314, clearly comparable to those observed with SU6656. Furthermore, continuous culture of NMuMG Fucci cells with SNS314 induced near identical multinucleated designs as with SU6656. To verify that SU6656 does indeed inhibit Aurora kinases we incubated control, SU6656, and SNS314 treated NIH3T3, E14/T and NMuMG Fucci cells with Demecolcine to inhibit mitosis in metaphase, a period where Aurora kinases are regarded as highly active, and measured the degrees of Aurora kinase driven histone H3 MAPK activation phosphorylation at serine 10 by immunocytochemistry and Western blotting. Our results show that 5 uM SU6656 inhibits Histone H3 phosphorylation nearly as potently as 1 uM SNS314 as shown by immunocytochemistry in NIH3T3 cells and Western blotting in E14/T and NMuMG Fucci cells, strongly suggesting that the effect induced by SU6656 within our different cell types is caused by cross specific inhibition of Aurora kinases as opposed to by its supposed inhibitory effect on the SFKs. As mentioned above we have used SU6656 to be able to examine the result of cYes inhibition on ES cell maintenance.