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

[EX Q]: Tumors of the nervous system most often occur in both children and adults as sporadic events with no family history of the disease, but they are also among the clinical manifestations of a significant number of familial cancer syndromes, including familial retinoblastoma, neurofibromatosis 1 and 2, tuberous sclerosis, and Cowden, Turcot, Li-Fraumeni and nevoid basal cell carcinoma (Gorlin) syndromes. All of these syndromes involve transmissible genetic risk resulting from loss of a functional allele, or inheritance of a structurally defective allele, of a specific gene. These genes include RB1, NF1, NF2, TSC1, TSC2, TP53, PTEN, APC, hMLH1, hPSM2, and PTCH, most of which function as tumor suppressor genes. The same genes are also observed in mutated and inactive forms, or are deleted, in tumor cells in sporadic cases of the same tumors. The nature of the mutational events that give rise to these inactivated alleles suggests a possible role of environmental mutagens in their causation. However, only external ionizing radiation at high doses is clearly established as an environmental cause of brain, nerve and meningeal tumors in humans. Transplacental carcinogenesis studies in rodents and other species emphasize the extraordinary susceptibility of the developing mammalian nervous system to carcinogenesis, but the inverse relationship of latency to dose suggests that low transplacental exposures to genotoxicants are more likely to result in brain tumors late in life, rather than in childhood. While not all neurogenic tumor-related genes in humans have similar effects in experimental rodents, genetically engineered mice (GEM) increasingly provide useful insights into the combined effects of multiple tumor suppressor genes and of gene-environment interactions in the genesis of brain tumors, especially pediatric brain tumors such as medulloblastoma.
[EX A]: Which is the gene mutated in type 1 neurofibromatosis?

[EX Q]: When reporter ANN MITCHELL is laid off by managing editor HENRY CONNELL because of streamlining, she begs to stay on since she's supporting her MOTHER and TWO SISTERS, but it's no use. Angry, she gathers up her belongings but then, as a parting shot, types up a fake letter from "John Doe" stating that he's so downtrodden by the unfairness of things that he intends jumping off the building on Christmas Eve.The paper prints the letter and it causes a sensation. Everyone relates to and wants to help John Doe. Connell, desperate to get hold of the original letter is shocked when Ann tells him there was no letter. Connell, angry, is ready to print a retraction but Ann suggests that they hire a "fake John Doe" to embody the pathos of the letter. She gets her job back along with a lucrative fee and contract.Several desperate MEN line up claming to have written the letter, so Ann and Connell must now pick the one. When handsome JOHN WILLOUGHBY walks in, Ann's clearly smitten. A likeable, quiet baseball player who's fallen on bad times, John's the one who will become "John Doe." Although he seems too honest to lie, Ann believes he's desperate enough. They create a fake letter, put him up at a fancy hotel with bodyguards, making him sign an agreement. Also in tow (much to Connell's chagrin) is THE COLONEL, a confirmed vagabond, distrustful of society, who warns John that he's falling into a trap of privilege.Next come publicity photos, which are directed by Ann to get the correct "angry protest" look. With headlines proclaiming his anger at the unfairness of the world, John becomes an increasing media sensation, courtesy of hyperbolic headlines concocted by Connell. Meanwhile, the GOVERNOR suspects John Doe is a myth but mistakenly feels it was concocted by publisher B. D. NORTON to discredit him. Ann convinces Norton to play it for what it's worth. Norton offers her money to write radio speeches to sell Doe. He also wants her to work directly with him and not Connell.Ann goes to work, typing up a storm but nothing comes to mind. Ann's Mother suggests that she write something upbeat and simple, using the values of Ann's late father as an inspiration. By now, John has begun realizing that his baseball career might not get started again if the John Doe business is revealed as a phony.Nonetheless, John reads his first manufactured upbeat speech, written by Ann to a packed house. Ann coaches him to be sincere, suggesting that she's fallen in love with John Doe. The speech, broadcast on the radio, stirs the people with its "love thy neighbor"-style message. CROWDS love him but John can't get away fast enough. He and the Colonel resort to the boxcars and flee. B. D. Norton, thinking he was great, wants him located.When a DINER WAITER recognizes him, John's hope for a return to normalcy is squelched by sudden CROWDS, eager to meet him. Ann and Norton locate him. John isn't happy about it. When Norton offers him a lecture tour, he refuses it angrily. When the common PEOPLE who have a "John Doe" club talk to him, however, he softens when hearing how he's touched them. Now, John's torn. His itinerant pal, The Colonel, thinks he's been "hooked" and, disgusted, walks out on him.Norton arranges the lecture tour. John speaks in state after state, addressing the many national clubs in his name. Connell tells Norton, however, that he's curious why Norton is spending so much money on the tour. In the meantime, Ann, knowing that John now likes her, feels increasingly like the heel she feels she is. She feels even worse when John relates a tender dream that he had about her and talks to her about how he relates to the lonely, hungry people to whom he's been speaking.Norton gives Ann a fur coat and a gift. He then tells her that he wants John Doe to announce a
[EX A]: Who plays the colonel?

[EX Q]: Antibody-mediated glomerulonephritis, including that resulting from immune complexes, is an important cause of renal failure and is in need of more specific and effective treatment. Binding of antibody or immune complexes to Fc receptors activates intracellular signal transduction pathways, including spleen tyrosine kinase (Syk), leading to the production of inflammatory cytokines. We examined the effect of R788 (fostamatinib disodium), an oral prodrug of the selective Syk inhibitor R406, in nephrotoxic nephritis in Wistar-Kyoto rats. Treatment with R788 reduced proteinuria, tissue injury, glomerular macrophage and CD8+ cell numbers, and renal monocyte chemoattractant protein-1 (MCP-1) and IL-1beta, even when we started treatment after the onset of glomerulonephritis. When we administered R788 from days 4 to 10, glomerular crescents reduced by 100% (P < 0.01) compared with the vehicle group. When we administered R788 treatment from days 7 to 14, established glomerular crescents reversed (reduced by 21%, P < 0.001), and renal function was better than the vehicle group (P < 0.001). In vitro, R406 downregulated MCP-1 production from mesangial cells and macrophages stimulated with aggregated IgG. These results suggest that Syk is an important therapeutic target for the treatment of glomerulonephritis.
[EX A]:
Which enzyme is inhibited by a drug fostamatinib?