Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Example Input: The susceptibility to arbekacin (ABK) of methicillin-resistant Staphylococcus aureus (MRSA) was investigated to find out how it related to aac(6')/aph(2") gene. In 49 isolates of MRSA for which MIC of ABK ranged from 0.125 to 64 micrograms/ml, the MICs of ABK for 38 strains carrying aac(6')/aph(2") gene were widely distributed from 0.25 to 64, whereas those for 11 strains without that gene were all < or = 0.5 microgram/ml. Residual rate of ABK activity was higher than that of gentamicin after the reaction with each crude enzyme preparation extracted from 3 isolates of MRSA, carrying aac(6')/aph(2") and aad(4',4") genes. Furthermore, 97 strains of MRSA isolated at Kanagawa prefecture in Japan in 1999 were all sensitive to ABK, although 28 strains of them carried aac(6')/aph(2") gene. These results showed that ABK resistance was not necessarily related to carrying aac(6')/aph(2") gene in clinical isolates of MRSA.
Example Output: What is MRSA?

Example Input: Chronic myeloid leukemia (CML) is arguably the best understood of all human malignancies. Its origins in the hematopoietic stem cell can be traced to a reciprocal translocation involving chromosomes 9 and 22, dubbed the Philadelphia chromosome, which is observed in essentially all patients. The resulting fusion gene, BCR/ABL, encodes an activated tyrosine kinase that can act alone to induce a CML-like syndrome in mouse models. These animal models have validated BCR/ABL as a target for the development of specific pharmaceutical inhibitors. The kinase inhibitor imatinib mesylate (Gleevec) is highly specific, effective, and minimally toxic, but may not effect cures as a single agent, particularly in patients with accelerated and blast-phase disease. Resistance to imatinib can confound therapy. Surprisingly, a high percentage of resistant cases manifest intact or augmented BCR/ABL signaling, suggesting that this oncoprotein, or signaling pathways emanating from it, remain viable targets. Combination chemotherapy is under active investigation, and among the most compelling strategies is dual treatment with agents that both target BCR/ABL signal transduction. BCR/ABL activates Ras, and compounds designed to antagonize Ras function called farnesyl transferase inhibitors (FTIs) have shown potent activity in vitro and in animal models of BCR/ABL-induced leukemia. Initial clinical trials in patients with refractory acute myeloid leukemia and CML in blast crisis have shown significant activity, suggesting that trials combining imatinib and FTIs are warranted.
Example Output: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?

Example Input: TabletSat-Aurora was launched from Dombarovsky (air base) site 13, Russia, on 19 June 2014 by a Dnepr-1 rocket.
Example Output:
What date was TabletSat-Aurora launched?