At the end of the eleventh century, with the collapse of Byzantine power after the Battle of Manzikert, Bitlis fell under the control of Togan Arslan, a subject of the Shah Arman (Also called Ahlatshah) dynasty based in Akhlat after brief Dilmachoglu rule. It was also ruled by Ayyubid (1207–1231), Khwarezm Shahs (shortly rule in 1230), Sultanate of Rûm (1231–1243) and Ilkhanate (1243–1335). Emirate
Bitlis was a Kurdish emirate from the 13th to the 19th century. Though often subordinate to a succession of larger powers that ruled the Van region, it always maintained a measure of independence. In the 14th century its emirs, the Kurdish Rusaki family, were vassals of the Karakoyunlu and the emirates territory also consisted of several smaller emirates: Ahlat, Mush, and Hinis. The emir of Bitlis submitted to Timur in 1394, but later helped the re-establishment of Karakoyunlu control in the region. After the collapse of the Karakoyunlu state, the Bitlis emirate disintegrated. However, in the 1470s it took the Aq Qoyunlu (White Sheep Turkomans) three successive sieges to capture Bitlis and in 1494/95 the Ruzaki recaptured the town. Armenians formed a large part of the citys population. A number of monasteries were permitted to be built by the Kurdish emirs and during the fifteenth century, Biltis flourished as a center for Armenian manuscript production. Bitlis was forced to accept a Persian governor during the invasion of the Safavid Shah Ismail, but sided with the Ottoman forces as they approached the region. Its emir, Sheref, later changed his allegiance to the Persians.
In 26 of 29 patients who met strict clinical criteria for the disorder, Lindhurst et al. identified an activating mutation in AKT1 kinase in a mosaic state gene.Previous research had suggested the condition linked to PTEN on chromosome 10, while other research pointed to chromosome 16. Prior to the findings regarding AKT1 in 2011, other researchers expressed doubt regarding the involvement of PTEN or GPC3, which codes for glypican 3 and may play a role in regulating cell division and growth regulation. Diagnosis
Differential diagnosis
Macrodystrophia lipomatosa
Fibrolipomatous hamartoma
Neurofibromatosis type 1
Klippel–Trénaunay syndrome
Parkes Weber syndrome
Sotos syndrome
Hemangiomas

Classification
Many sources classify Proteus syndrome to be a type of nevus syndrome. The lesions appear to be distributed in a mosaic manner. It has been confirmed that the disorder is an example of genetic mosaicism. Treatment
A team of doctors in Australia have trial tested the drug rapamycin in the treatment of a patient said to have Proteus syndrome and have found it to be an effective remedy. However, the diagnosis of Proteus syndrome in this patient has been questioned by others.The Proteus syndrome research team in the National Human Genome Research Institute at the United States National Institutes of Health have initiated a Phase 0 dose finding trial with the AKT1 inhibitor ARQ 092, which is being developed by the Arqule Corporation. In earlier tests on tissue and cell samples obtained from patients, ARQ 092 reduced phosphorylation of AKT and downstream targets of AKT in as little as two hours. The Phase 0 trial opened in November 2015.