Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.

Ex Input:
Context: Autosomal-recessive hereditary spastic paraplegias (AR-HSP) consist of a genetically diverse group of neurodegenerative diseases characterised by pyramidal tracts dysfunction. The causative genes for many types of AR-HSP remain elusive. We tried to identify the gene mutation for AR-HSP with cerebellar ataxia and neuropathy. This study included two patients in a Japanese family with their parents who are first cousins. Neurological examination and gene analysis were conducted in the two patients and two normal family members. We undertook genome-wide linkage analysis employing single nucleotide polymorphism arrays using the two patients' DNAs and exome sequencing using one patient's sample. We detected a homozygous missense mutation (c.4189T>G, p.F1397V) in the lysosomal trafficking regulator (LYST) gene, which is described as the causative gene for Chediak-Higashi syndrome (CHS). CHS is a rare autosomal-recessive syndrome characterised by hypopigmentation, severe immune deficiency, a bleeding tendency and progressive neurological dysfunction. This mutation was co-segregated with the disease in the family and was located at well-conserved amino acid. This LYST mutation was not found in 200 Japanese control DNAs. Microscopic observation of peripheral blood in the two patients disclosed large peroxidase-positive granules in both patients' granulocytes, although they had no symptoms of immune deficiency or bleeding tendency. We diagnosed these patients as having adult CHS presenting spastic paraplegia with cerebellar ataxia and neuropathy. The clinical spectrum of CHS is broader than previously recognised. Adult CHS must be considered in the differential diagnosis of AR-HSP.
Question: Which mutated gene causes the ChediakHigashi Syndrome?

Ex Output:
lysosomal trafficking regulator gene

Ex Input:
Context: Hoping to rebound from a divisional home loss to the Eagles, the Cowboys flew to Bank of America Stadium for a Week 16 Saturday night duel with the Carolina Panthers. In the first quarter, Dallas shot first with QB Tony Romo completing a 10-yard TD pass to WR Terrell Owens for the only score of the period. In the second quarter, the 'Boys continued their assault as RB Marion Barber got a 5-yard TD run. The Panthers would get on the board with QB Matt Moore completing an 11-yard TD pass to WR Steve Smith. The Cowboys end the half with rookie kicker Nick Folk getting a 42-yard field goal. In the third quarter, Carolina started to try a comeback as kicker John Kasay getting a 37-yard field goal for the only score of the period. In the fourth quarter, Dallas would respond with Folk kicking a 23-yard field goal. The Panthers tried to rally as Kasay nailing a 25-yard field goal, yet the 'Boys were able to hold off every possible attempt. With the win, the Cowboys improved to 13-2 and clinched homefield through NFC Playoffs with Green Bay's loss to Chicago on Sunday. Terrell Owens (5 receptions for 48 yards and 1 touchdown) left the game in the second quarter with a high left ankle sprain.
Question: What was the shortest field goal made?

Ex Output:
23-yard

Ex Input:
Context: Chronic myeloid leukemia (CML) is characterized by formation of a BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22. Recently the development of new fluorescence in-situ hybridization (FISH) techniques has allowed identification of unexpected deletions of the reciprocal translocation product, the derivative chromosome 9, in 10% to 15% of patients with CML. These deletions are large, span the translocation breakpoint, and occur at the same time as the Ph translocation. Such deletions therefore give rise to previously unsuspected molecular heterogeneity from the very beginning of this disease, and there is mounting evidence for similar deletions associated with other translocations. Several studies have demonstrated that CML patients who carry derivative chromosome 9 deletions exhibit a more rapid progression to blast crisis and a shorter survival. Deletion status is independent of, and more powerful than, the Sokal and Hasford/European prognostic scoring systems. The poor prognosis associated with deletions is seen in patients treated with hydroxyurea or interferon, and preliminary evidence suggests that patients with deletions may also have a worse outcome than nondeleted patients following stem cell transplantation or treatment with imatinib. Poor outcome cannot be attributed to loss of the reciprocal ABL-BCR fusion gene expression alone, and is likely to reflect loss of one or more critical genes within the deleted region. The molecular heterogeneity associated with the Philadelphia translocation provides a new paradigm with potential relevance to all malignancies associated with reciprocal chromosomal translocations and/or fusion gene formation.
Question: Which gene fusion is the result of the "philadelphia translocation" or the "philadelphia chromosome" mutation?

Ex Output:
the bcr/abl gene fusion