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

Example Input: Facioscapulohumeral muscular dystrophy (FSHD) is a primary muscle disorder with autosomal dominant inheritance. FSHD was mapped to chromosome 4 locus q35, but the gene is not yet known. It is characterised by progressive, often asymmetric, selective muscular weakness and great clinical variability. The aim of the study was to analyze 62 FSHD cases from 44 Polish families in which the diagnosis was confirmed by DNA analyses. FSHD diagnosis was based on the clinical findings and standardized investigations confirming primary muscular involvement (EMG, muscle biopsy). DNA analysis was based on EcoRI/BlnI restriction enzyme digestion followed by hybridization with P13E-11 molecular probe. In our material, we have found a relatively large percentage (41%) of big deletions (EcoRI/BlnI fragment of 10-15 kb [kilo bases]), which in the majority of cases (67%) was present in isolated cases. In 10 families (23%) the phenotype was assessed as severe. These are cases with the onset before the age of 10 and fast progression. "Middle sized" deletions (EcoRI/BlnI fragment of 16-29 kb) were prevalent in familial cases and present in 57% of families. "Small" deletion was found in one family (EcoRI/BlnI fragment of 30 kb). Somatic mosaicism was confirmed in one case. De novo mutations were shown in 11% of the examined families. The results of this study indicate that the bigger the deletion, the more severe the FSHD course, however there are some exceptions. A similar relationship has been shown by previous research. Molecular analyses are particularly important in atypical and sporadic cases. It is the first genetic presentation of a group of patients' with this kind of dystrophy in the Polish population.
Example Output: What is the mode of inheritance of Facioscapulohumeral muscular dystrophy (FSHD)?

Example Input: CADASIL is a cerebrovascular disease caused by mutations in the NOTCH3 gene. Most mutations result in a gain or loss of cysteine residue in one of the 34 epidermal growth factor-like repeats in the extracellular domain of the Notch3 protein, thus sparing the number of cysteine residues. To date, more than 130 different mutations in the NOTCH3 gene have been reported in CADASIL patients, of which 95% are missense point mutations. Many polymorphisms have also been identified in the NOTCH3 coding sequence, some of them leading to amino acid substitutions. The aim of the present study was to analyze the NOTCH3 gene in a large group of patients affected by leukoencephalopathy and to investigate the presence of genetic variants. The molecular analysis revealed several nucleotide alterations. In particular, we identified 20 different mutations, 22 polymorphisms, and 8 genetic variants of unknown pathological significance never reported previously. We hope that this NOTCH3 gene mutational analysis, performed in such a significant number of unrelated and related patients affected by leukoencephalopathy, will help in molecular screening for the NOTCH3 gene, thus contributing to enlargement of the NOTCH3 gene variation database.
Example Output: Which amino acid residue appears mutated in most of the cases reported with  cadasil syndrome?

Example Input: Two forms of the inherited long QT syndrome have been known for many years: the autosomal recessive Jervell and Lange-Nielsen form and the autosomal dominant Romano-Ward form. A gene marker at the 11p 15.5 locus has been identified for some, but not all, families with the autosomal dominant form, but as yet the gene has not been identified. It is apparent that mutations of at least four genes, and possibly more, can cause the syndrome. The molecular biology of the syndrome is not yet clarified, but abnormalities of ion channel function are likely, particularly the potassium delayed rectifier current. Proposals for the pathophysiology include an abnormality of a G protein which controls ion channel and adrenergic pathway function, as well as a disturbance of the sympathetic nervous system. The identification of the abnormal gene(s) and the gene products will provide precise information on the molecular physiology of the syndrome.
Example Output:
What is the mode of inheritance of Romano Ward long QT syndrome?