It is possible this favorable hydrophobic packing interaction might explain why PHA 739358 is more active from the mutant than the WT protein. PHA 739358 can represent a valuable book agent to target the T315I Bcr Abl mutation, (-)-MK 801 and preclinical and clinical data are coming through to support this concept. Results The T315I is in charge of approximately 15% of the cases of relapse in CML and Ph ALL individuals on therapy. The clinical relevance with this mutant probably will increase significantly regarding date it appears to represent the key mechanism of resistance to nilotinib and dasatinib, the second era inhibitors already being developed clinically. Architectural Chromoblastomycosis studies suggest that the substitution of threonine with isoleucine at residue 315 eliminates an essential hydrogen bonding interaction and features a steric clash which abrogates efficient and binding inhibition of Bcr Abl by imatinib in addition to by several novel inhibitors. A possible approach to the development of second-line strategies overcoming resistance caused by the mutation is to design inhibitors binding elements of Bcr Abl besides the ATP binding pocket. An intriguing alternative is to explore the likelihood of whether elements which have been produced as inhibitors for other protein kinases and are already undergoing clinical trials might range from the T315I Bcr Abl mutant among their off targets. Even though off target exercise may bring about undesirable side effects, it’s to be recognized that emphasizing compounds that already are being tested in clinical practice may speed up the development of successful therapeutic strategies. Recent studies have shown that MK 0457 and PHA 739358, two small molecule aurora kinase inhibitors, have in vitro activity against the T315I Bcr Abl. More over, initial data showed promising clinical effectiveness in patients afflicted with Philadelphia good leukemias, relapsing or resistant to first and second generation TK inhibitors. Such Dovitinib clinical trial an amazing efficacy raises the issue of whether aurora kinases may also harbor some pathogenetic significance in CML and/or Ph ALL or may be precisely deregulated by the T315I Bcr Abl, and whether auroras may be considered a suitable secondary target for inhibition. To evaluate which type of anti-hypertensive agents promote the growth or the manifestation of type 2 diabetes mellitus. How high is the incidence of new onset diabetes during antihypertensive therapy and how is treatment induced type 2 diabetes mellitus evaluated clinicallyfi Which agents are therefore affordable in the long termfi Which honest, social or legal aspects must be regardedfi Methods A systematic literature review was performed including clinical trials with at least five participants which reported new onset diabetes in the course of antihypertensive treatment.