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

[Q]: Coming off their last-second victory over the Bengals, the Broncos would play their Week 2 home opener against the Cleveland Browns. In the first quarter, Denver would trail early as Browns kicker Phil Dawson got a 22-yard field goal. Afterwards, the Broncos took the lead as quarterback Kyle Orton completed a 2-yard touchdown pass to tight end Tony Scheffler. Cleveland would creep close as Dawson made a 47-yard field goal, but Denver would answer as kicker Matt Prater got a 23-yard field goal in the second quarter and a 38-yard field goal in the third quarter. In the fourth, the Broncos pulled away as fullback Peyton Hillis got a 2-yard touchdown run and running back Correll Buckhalter got a 45-yard touchdown run.
[A]: Which player kicked the second longest field goal?

[Q]: 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.
[A]: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?

[Q]: To assess the efficacy and safety of R788 (fostamatinib disodium), an inhibitor of spleen tyrosine kinase (Syk), in patients with active rheumatoid arthritis (RA) that did not respond to biologic therapies. A total of 219 patients with active RA in whom treatment with biologic agents had failed were enrolled in a 3-month multicenter, randomized, double-blind, placebo-controlled trial of R788. The primary end point was the percentage of patients who met the American College of Rheumatology 20% improvement criteria (achieved an ACR20 response) at month 3. Secondary end points included changes in inflammation and damage, as assessed by magnetic resonance imaging (MRI), and changes in the Disease Activity Score. The ACR20 response in the R788 100 mg twice daily group was 38%, versus 37% in the placebo group, at month 3. No significant differences were achieved in the ACR20, ACR50, or ACR70 response levels at 3 months. There were differences between the groups from baseline to month 3 in the secondary end points C-reactive protein (CRP) level and synovitis score on MRI. There were baseline differences in steroid use, prior biologic use, and synovitis score on MRI between the R788 group and the placebo group that may have affected the outcomes. A high placebo response rate was seen in this trial, and exploratory analysis suggested that this may in part have been driven by patients who entered the trial with an elevated erythrocyte sedimentation rate but normal CRP level. Our findings indicate that there were no differences in the primary end point between the R788 and placebo groups. Differences were observed between the R788 and placebo groups in secondary end points, particularly in those patients who entered the study with an elevated CRP level.
[A]:
Which enzyme is inhibited by a drug fostamatinib?