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 are a high school senior graduating and looking to enter college in 2006, you will take the new exam. The biggest change to the SAT will be the introduction of a new writing section. The writing section will consist of two parts: an essay and a multiple-choice section. Students will be given 25 minutes to respond to a prompt and construct a well-organized essay that effectively deals with the task. The essay question may require students to complete a statement, to react to a quote, or to agree or disagree with a point of view. In any case, a good essay will support the chosen position with specific reasons and examples from literature, history, art, science, current affairs, or even a student's own experiences. Essays will be scored based on the procedures for the current SAT II: Writing Test. Essays will be graded by two independent readers On a scale of 1~6, and their two scores will be combined to form an essay subscore that ranges from 2 to 12. Should the readers' scores vary by more than 2 points, a third reader will score the essay; The readers will be high school teachers and college professors who teach composition. To ensure that essays will be scored in a timely manner, they will be scanned and made available to readers on the Internet for grading purpose. The writing section will also include multiple-choice grammar and usage questions. Some of these questions will call upon students to improve given sentences and paragraphs. Others will present students with sentences and require them to identify mistakes in diction , grammar, sentence construction, subject-verb agreement, proper word usage. The highest possible score on the new writing section will be 800. Scores on the essay and multiple-choice section will be combined to produce a single score. A writing subscore will also be assigned. The highest possible scores on the Critical Reading and Math sections will remain 800 each, making 2,400 a perfect score on the new SAT.
[EX A]: Which parts are included in the writing section of SAT according to the passage?

[EX Q]: In melanoma, transition to the vertical growth phase is the critical step in conversion to a deadly malignant disease. Here, we offer the first evidence that an antioxidant enzyme has a key role in this transition. We found that the antioxidant enzyme peroxiredoxin-2 (Prx2) inversely correlated with the metastatic capacity of human melanoma cells. Silencing Prx2 expression stimulated proliferation and migration, whereas ectopic expression of Prx2 produced the opposite effect. Mechanistic investigations indicated that Prx2 negatively regulated Src/ERK activation status, which in turn fortified adherens junctions function by increasing E-cadherin expression and phospho-Y654-dependent retention of -catenin in the plasma membrane. In murine melanoma cells, Prx2 silencing enhanced lung metastasis in vivo. Interestingly, the natural compound gliotoxin, which is known to exert a Prx-like activity, inhibited proliferation and migration as well as lung metastasis of Prx2-deficient melanoma cells. Overall, our findings reveal that Prx2 is a key regulator of invasion and metastasis in melanoma, and also suggest a pharmacologic strategy to effectively decrease deadly malignant forms of this disease.
[EX A]: What type of enzyme is peroxiredoxin 2 (PRDX2)?

[EX Q]: The product of the multiple endocrine neoplasia type 1 (MEN1) tumor suppressor gene, menin, is an integral component of MLL1/MLL2 histone methyltransferase complexes specific for Lys4 of histone H3 (H3K4). We show that menin is a transcriptional coactivator of the nuclear receptors for estrogen and vitamin D. Activation of the endogenous estrogen-responsive TFF1 (pS2) gene results in promoter recruitment of menin and in elevated trimethylation of H3K4. Knockdown of menin reduces both activated TFF1 (pS2) transcription and H3K4 trimethylation. In addition, menin can directly interact with the estrogen receptor-alpha (ERalpha) in a hormone-dependent manner. The majority of disease-related MEN1 mutations prevent menin-ERalpha interaction. Importantly, ERalpha-interacting mutants are also defective in coactivator function. Our results indicate that menin is a critical link between recruitment of histone methyltransferase complexes and nuclear receptor-mediated transcription.
[EX A]:
Which is the histone residue methylated by MLL1?