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

[EX Q]: If you wish to become a better reader, here are four important things to remember about reading _ : * Knowing why you are reading or what you are reading to find out will often help you to know whether to read rapidly or slowly. * Some things should be read slowly throughout. Examples are directions for making or doing something, arithmetic problems, science and history books, which are full of important information. You must read such things slowly to remember each important step and understand each important ideas. * Some things should be read rapidly throughout. Examples are simple stories meant for enjoyment, news letters from friends, pieces of news from local, or home-town, papers, telling what is happening to friends and neighbors. * In some of your reading, you must change your speed from fast to slow and slow to fast, as you go along. You will need to read certain pages rapidly and then slow down and do more careful reading when you come to important ideas which must be remembered.
[EX A]: Which should be read slowly according to the passage?

[EX 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.
[EX A]: Which human disease is associated with mutated UBQLN2

[EX Q]: Tumors of the central nervous system are the most frequent solid tumors in childhood. With 30-40% of this heterogenous group, low-grade astrocytomas represent the most common subtype. Neurofibromatosis type 1 (NF1) is strongly associated with the development of pilocytic astrocytoma (PA), frequently appearing as optic glioma. Neurofibromatosis 1 gene (NF1 ) fulfills the criteria of a tumor suppressor gene and is deleted or mutated heterozygously in patients with NF1. This suggests an involvement in the development of PA. To clarify whether silencing of NF1 by promoter methylation plays a role in PA and especially in optic glioma, the authors investigated the methylation status in 30 PA, 6 of which had optic glioma. However, no methylation was found at the NF1 promoter region in PA. To rule out that silencing of NF1 by promoter methylation is restricted to higher-grade astrocytomas, 15 pediatric WHO II degree and IV degree astrocytomas were analyzed: 12 astrocytomas II and 3 glioblastomas displayed no NF1 promoter methylation. The authors conclude that NF1 silencing by methylation plays no role in low-grade astrocytoma.
[EX A]:
Which is the gene mutated in type 1 neurofibromatosis?