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

Q: Chronic myeloid leukemia (CML) is caused by Bcr-Abl, a constitutively active tyrosine kinase that is the result of a reciprocal translocation between chromosomes 9 and 22 and cytogenetically evident as the Philadelphia chromosome. Imatinib (Glivec, Gleevec), a specific small molecule inhibitor of Bcr-Abl, has become the standard drug therapy for CML, and has dramatically diminished the use of allogeneic stem cell transplantation. Despite unprecedented rates of complete cytogenetic response, residual disease remains detectable in the majority of patients, suggesting that imatinib fails to eradicate leukemic stem cells. In this publication, the current perspectives for CML patients treated with imatinib are reviewed, focusing on the results of both standard and high-dose therapy. Monitoring of time-dependent prognostic factors is reviewed. The reasons imatinib may not be able to eradicate the disease are discussed, and potential strategies to achieve disease elimination are presented. Lastly, resistance to imatinib and the potential of second-generation Abl kinase inhibitors in the setting of clinical resistance are considered.

A: What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?
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Q: Chediak-Higashi syndrome (CHS) is a rare multiorgan disease entity with autosomal recessive inheritance characterized by oculocutaneous albinism, bleeding tendency, recurrent bacterial infections and various neurological symptoms. Intracellular vesicle formation is deficient, resulting in giant granules in many cells, e.g. giant melanosomes in the melanocytes. Diagnosis has been based on morphological examination of peripheral blood and bone marrow, with giant granules seen in cells of the myeloid lineage and in lymphocytes. The ultimate diagnostic test is to look for a mutated LYST gene. Most patients develop an accelerated phase of the disease with deposition of lymphohistiocytes in the liver, spleen, lymph nodes and bone marrow, resulting in hepatosplenomegaly, bone marrow infiltration and haemophagocytosis. Peripheral blood neutropenia becomes more profound as anaemia and thrombocytopenia develop. Most patients succumb before the age of 10 years. Four patients with CHS are described, one of whom is a long-term survivor after successful allogeneic bone marrow transplantation, two succumbed during the accelerated phase and one is living with a chronic form of the disease. Allogeneic bone marrow transplantation from an HLA-matched sibling is the therapy of choice and should be performed early. If there is no matched family donor, an unrelated donor or a placental blood graft is a good alternative. The clinical picture of CHS is heterogeneous and therapeutic decisions need to be made on an individual basis.

A: Which mutated gene causes the ChediakHigashi Syndrome?
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Q: On July 24, 2017, Gasol re-signed with the Spurs. On December 20, 2017, he had 20 points and a season-high 17 rebounds in a 93-91 win over the Portland Trail Blazers. On December 23, 2017, he recorded his 10th career triple-double with 14 points, 11 rebounds and a season-high 10 assists in a 108-99 win over the Sacramento Kings. On December 26, 2017, in a 109-97 win over the Brooklyn Nets, Gasol collected his 10,817th rebound, moving him past Jack Sikma for 30th in league history. On January 26, 2018, in a 97-78 loss to the Philadelphia 76ers, Gasol became the 34th player in NBA history to play 40,000 career minutes. On March 25, 2018, he had 22 points on 10-of-15 shooting and grabbed 13 rebounds in a 106-103 loss to the Milwaukee Bucks.

A:
Did Gasol's team score more points against the Brooklyn Nets or the Milwaukee Bucks?
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