which may include deafness as part of the picture. TMPRSS3 gene was identified by its association with both congenital and childhood onset autosomal recessive deafness. This gene is expressed in fetal cochleae and many other tissues, and is thought to be involved in the development and maintenance of the inner ear or the contents of the perilymph and endolymph. It was also identified as a tumor associated gene that is overexpressed in ovarian tumors. Charcot–Marie–Tooth disease an inherited neurological disorder with delayed onset that can affect the ears as well as other organs. The hearing loss in this condition is often ANSD (auditory neuropathy spectrum disorder) a neural cause of hearing loss. Muckle–Wells syndrome, a rare inherited autoinflammatory disorder, can lead to hearing loss. Autoimmune disease: although probably rare, it is possible for autoimmune processes to target the cochlea specifically, without symptoms affecting other organs. Granulomatosis with polyangiitis, an autoimmune condition, may precipitate hearing loss. Congenital Infections: Congenital rubella syndrome, CRS, results from transplacental transmission of the rubella virus during pregnancy. CRS has been controlled by universal vaccination (MMR or MMRV vaccine). Cytomegalovirus (CMV) infection is the most common cause of progressive sensorineural hearing loss in children. It is a common viral infection contracted by contact with infected bodily fluids such as saliva or urine and easily transmitted in nurseries and thus from toddlers to expectant mothers. CMV infection during pregnancy can affect the developing foetus and lead to learning difficulties as well as hearing loss. Toxoplasmosis, a parasitic disease affecting 23% of the population in the U.S., can cause sensorineural deafness to the fetus in utero. Hypoplastic auditory nerves or abnormalities of the cochlea. Abnormal development of the inner ear can occur in some genetic syndromes such as LAMM syndrome (labyrinthine aplasia, microtia and microdontia), Pendred syndrome, branchio-oto-renal syndrome, CHARGE syndrome GATA2 deficiency, a grouping of several disorders caused by common defect, viz., familial or sporadic inactivating mutations in one of the two parental GATA2 genes. These autosomal dominant mutations cause a reduction, i.e. a haploinsufficiency, in the cellular levels of the gene's product, GATA2. The GATA2 protein is a transcription factor critical for the embryonic development, maintenance, and functionality of blood-forming, lympathic-forming, and other tissue-forming stem cells. In consequence of these mutations, cellular levels of GATA2 are deficient and individuals develop over time hematological, immunological, lymphatic, and/or other disorders. GATA2 deficiency-induced abnormalities in the lymphatic system are proposed