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 Q]: Context: The launch occurred on 12 June 1970 at 09:30:02 UTC, and resulted in the successful deployment of Kosmos 347 into low Earth orbit. 
 Question: What date was Kosmos 347 launched?
[EX A]: 12 june 1970

[EX Q]: Context: This article's plot summary may be too long or excessively detailed. Please help improve it by removing unnecessary details and making it more concise. (October 2011) (Learn how and when to remove this template message) Oyuki, a tattooed female assassin the renegade member of a daimyo's personal bodyguard detail is killing every man that is sent up against her. Along with her deadly use of the short blade, she strips to the waist while fighting to reveal elaborate tattoos on her chest and back. On her front is a kintaro grasping her left breast. A portrait of a mountain witch covers her back. She then cuts off her victims' topknots, or chonmage, which brings dishonor to the dead man and his family. Ogami Itto, the disgraced former shogun's executioner, or Kogi Kaishakunin, is hired to kill Oyuki. He tracks down the tattoo artist, who explains that she was a "fine" woman who did not scream as he dug into her flesh with his needles. Meanwhile, Itto's 3-year-old son, Daigoro, has grown restless waiting by the baby cart his father uses to trundle him about in. He goes exploring and finds a pair of performing clowns on the street. When the clowns finish their performance, Daigoro follows them, hoping to see more. But the clowns shoo him away, saying it's time to go home. Now, Daigoro has wandered too far. He is lost, and has become separated from his father. Agents of the Ogamis' mortal enemies, the Yagyu, are never far away. A procession of them, accompanied by the sound of gongs and loud shrieks, sends Daigoro into hiding. Itto must give up his search rather than risk an entanglement with the men, so he travels on alone. Daigoro spends days looking for his father, searching in every temple in the countryside. He enters one temple and sees a figure at the altar praying, but it is not his father. Rather, it is a man whom Daigoro immediately recognizes as someone who is unfriendly. The man follows Daigoro, who wanders into a grass field as it is being lit on fire by farmers. Unwittingly, Daigoro is surrounded by the flames, but he proves his resourcefulness by burying himself and surviving. The man then turns his sword on Daigoro, who raises a stick to defend himself, and in that instant the man realizes who Daigoro is. Just then, Itto comes into the picture, and the two recognize each other. The man, it turns out is Gunbei Yagyu, the outcast son of Retsudo Yagyu. Gunbei and Itto had competed for the post of shogun's executioner, and Gunbei's fierce swordsmanship surely would have won him the post, but in his over zealousness, he ends up pointing his sword at the shogun a taboo movement that costs him the job and makes him an outcast. Itto and Gunbei now have a rematch, but Itto is much improved and is ready for Gunbei. With a swift stroke, he chops off Gunbei's right arm. Gunbei then begs Itto to kill him, but Itto refuses, saying there is nothing to be gained from slaying a man who is already dead. With Gunbei out of the way and father and son reunited, the action then turns on finding the tattooed killer, Oyuki. He first stops at a settlement of street actors that Oyuki was said to be a part of. He talks to the elder and hears more of her story, and it happens that the elder is Oyuki's father, who is opposed to her actions, and cooperates with Itto. Itto finally locates Oyuki at a hot spring and witnesses her in action against more vassals who have come to try to kill her. Then her nemesis, her former instructor who raped her and set her on her bloody vendetta, shows up with his flaming sword and blazing eyes. But she is no longer in his sway, and when he sees her tattoos, he is distracted and killed. Finally, Itto and Oyuki must duel, and he makes quick work of her. She dies a splendid 
 Question: Of what is the portrait that covers her back?
[EX A]: a mountain

[EX Q]: Context: The acromelic dysplasia group is characterized by short stature, short hands and feet, stiff joint, and "muscular" build. Four disorders can now be ascribed to this group, namely Weill-Marchesani syndrome (WMS), geleophysic dysplasia (GD), acromicric dysplasia (AD), and Myhre syndrome (MS). Although closely similar, they can be distinguished by subtle clinical features and their pattern inheritance. WMS is characterized by the presence of dislocation of microspherophakia and has autosomal dominant or recessive mode of inheritance. GD is the more severe one, with a progressive cardiac valvular thickening, tracheal stenosis, bronchopulmonary insufficiency, often leading to an early death. AD has an autosomal dominant mode of inheritance, distinct facial and skeleton features (a hoarse voice and internal notch of the femoral head). Finally, MS is sporadic, characterized by prognathism, deafness, developmental delay, thickened calvarium, and large vertebrae with short and large pedicles. We first identified mutations in Fibrillin-1 (FBN1) in the dominant form of WMS and then mutations in A Disintegrin-like And Metalloproteinase domain with ThromboSpondin type 1 repeats 10 (ADAMTS10) in the recessive form of WMS. The function of ADAMTS10 is unknown but these findings support a direct interaction between ADAMTS10 and FBN1. We then identified mutations in ADAMTSL2 in the recessive form of GD and a hotspot of mutations in FBN1 in the dominant form of GD and in AD (exon 41-42, encoding TGF binding protein-like domain 5 (TB5) of FBN1). The function of ADAMTSL2 is unknown. Using a yeast double hybrid screen, we identified latent transforming growth factor- (TGF) binding protein 1 as a partner of ADAMTSL2. We found an increased level of active TGF in the fibroblast medium from patients with FBN1 or ADAMTSL2 mutations and an enhanced phosphorylated SMAD2 level, allowing us to conclude at an enhanced TGF signaling in GD and AD. Finally, a direct interaction between ADAMTSL2 and FBN1 was demonstrated suggesting a dysregulation of FBN1/ADAMTSL2 interrelationship as the underlying mechanism of the short stature phenotypes. Using exome sequencing in MS probands, we identified de novo SMAD4 missense mutations, all involving isoleucine residue at position 500, in the MH2 domain. In MS fibroblasts, we found decreased ubiquitination level of SMAD4 and increased level of SMAD4 supporting a stabilization of SMAD4 protein. Functional SMAD4 is required for canonical signal transduction through the oligomerization with phosphorylated SMAD2/3 and SMAD1/5/8. We therefore studied the nuclear localization of mutant SMAD complexes and found that the complexes translocate to the nucleus. We finally observed a decreased expression of downstream TGF target genes supporting impaired TGF driven transcriptional control in MS. Our findings support a direct link between the short stature phenotypes and the TGF signaling. However, the finding of enhanced TGF signaling in Marfan phenotypes supports the existence of yet unknown mechanisms regulating TGF action. 
 Question: What is the mode of inheritance of Acromicric dysplasia?
[EX A]:
autosomal dominant