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

Q: Heavily in debt, Clinton lobbied the Duke of Newcastle for profitable employment as an American governor: he was appointed Governor of the Province of New York in July 1741 and arrived in New York in September 1743 to take up his position. Promoted to rear-admiral on 10 December 1743 and vice-admiral on 23 June 1744, he sought to protect New York's Northern border from attack by the French: however liberal members of the New York assembly resisted his proposals as they wanted to maintain trade links with the French and with the Native Americans who were under French influence. James De Lancey, who had initially been his main adviser, turned against him and sought to block the governor's salary. Clinton therefore invited Sir William Johnson to take over responsibility for Native American affairs in 1746 and appointed Cadwallader Colden to be his advisor. Clinton was promoted to full admiral on 15 July 1747. Working with the Mohawk chief Hendrick Theyanoguin, Johnson was able to recruit Mohawk warriors to fight on the side of the British in 1747 during King George's War. After continuing disputes with the assembly over military expenditure and payment of the governor's salary, Clinton resigned as governor in October 1753.

A: What happened second: Clinton was appointed Governor or promoted to rear-admiral?
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Q: Amyotrophic Lateral Sclerosis (ALS) is the most frequent motor neuron disease in adults. Classical ALS is characterized by the death of upper and lower motor neurons leading to progressive paralysis. Approximately 10% of ALS patients have familial form of the disease. Numerous different gene mutations have been found in familial cases of ALS, such as mutations in superoxide dismutase 1 (SOD1), TAR DNA-binding protein 43 (TDP-43), fused in sarcoma (FUS), C9ORF72, ubiquilin-2 (UBQLN2), optineurin (OPTN) and others. Multiple animal models were generated to mimic the disease and to test future treatments. However, no animal model fully replicates the spectrum of phenotypes in the human disease and it is difficult to assess how a therapeutic effect in disease models can predict efficacy in humans. Importantly, the genetic and phenotypic heterogeneity of ALS leads to a variety of responses to similar treatment regimens. From this has emerged the concept of personalized medicine (PM), which is a medical scheme that combines study of genetic, environmental and clinical diagnostic testing, including biomarkers, to individualized patient care. In this perspective, we used subgroups of specific ALS-linked gene mutations to go through existing animal models and to provide a comprehensive profile of the differences and similarities between animal models of disease and human disease. Finally, we reviewed application of biomarkers and gene therapies relevant in personalized medicine approach. For instance, this includes viral delivering of antisense oligonucleotide and small interfering RNA in SOD1, TDP-43 and C9orf72 mice models. Promising gene therapies raised possibilities for treating differently the major mutations in familial ALS cases.

A: Which human disease is associated with mutated UBQLN2
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Q: Increased nerve growth factor levels are associated with chronic pain conditions, including chronic low back pain (LBP). This study examined safety and analgesic efficacy of tanezumab, a humanized anti-nerve growth factor antibody, in adults with chronic LBP. Patients received intravenous tanezumab 200 g/kg plus oral placebo (n=88), intravenous placebo plus oral naproxen 500 mg twice a day (n=88), or intravenous placebo plus oral placebo (n=41). Primary outcome was average LBP intensity (aLBPI) at Week 6. Secondary outcomes were proportion of patients with 30% or 50% reduction in aLBPI, Roland-Morris Disability Questionnaire and Brief Pain Inventory-short form scores, Patients' Global Assessment of LBP, Patients' Global Evaluation of study medication, and rescue medication use. Mean aLBPI change from baseline to Week 6 was greater with tanezumab vs naproxen (P=0.004) and placebo (P<0.001). Greater proportions of patients reported 30% and 50% reduction in aLBPI with tanezumab vs naproxen (P0.013) and placebo (P<0.001), and greater improvements in Roland-Morris Disability Questionnaire (P<0.001) and other secondary outcomes except rescue medication use. Tanezumab was associated with adverse events (AEs) of abnormal peripheral sensation that were generally mild and resolved before study completion; however, there were no serious AEs. Nine patients (4 of whom were tanezumab-treated) discontinued due to AEs. In conclusion, tanezumab resulted in analgesic efficacy that was clinically and statistically superior to placebo and naproxen in patients with chronic LBP. Tanezumab clinical development is on regulatory hold due to AEs in osteoarthritis patients.

A:
What is the target of tanezumab?
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