It has been noted that a leading hypothesis for the pathogenesis of Kawasaki disease also involves a hyperinflammatory response to viral infection (such as by a novel RNA virus) in some genetically predisposed children, and that SARS-CoV-2 is now "added to the list" of implicated viral triggers. Hopes have been expressed that study of the new condition may help understand the hidden mechanisms behind Kawasaki disease. But current evidence suggest that MIS-C and Kawasaki disease represent two distinct disease entities

Proposed role of the STING pathway
A possible role of the stimulator of interferon genes known as STING has been proposed. SARS-CoV-2 is capable of upregulating the STING protein (encoded by TMEM173 transmembrane protein, and expressed in alveoli, endothelial cells, and the spleen), resulting in massive release of interferon-beta and cytokines derived from activation of NF-κB and IRF-3. In MIS-C, such a scenario could lead to a clinical picture similar to STING-associated vasculopathy with onset in infancy (also known as SAVI) – a condition characterized by fever, lung injury, vascular inflammation, myositis, skin lesions (occasionally acral necrosis), and arterial aneurysms. Variations in the presentation and severity of MIS-C might at least partially be explained by characteristic differences in polymorphisms of TMEM173 found in various populations. Epidemiology
Epidemiological information is limited, and clinical statistics currently derive from review of case series. This emerging condition is considered rare. Its incidence is not known.
Otofaciocervical syndrome, also known as Fara Chlupackova syndrome, are a small group of rare developmental disorders of genetic origin which are characterized by facial dysmorphisms, long neck, preauricular and/or branchial pits, cervical muscle hypoplasia, hearing loss, and mild intellectual disabilities. Additional findings include vertebral anomalies and short stature. Types
There are two types of OFC:

Otofaciocervical syndrome type 1
It is characterized by facial dysmorphisms, low-set cup-shaped ears, preauricular sinus or cyst, hearing loss, branchial and skeletal anomalies, low-set clavicle bones, winged scapulae, sloping shoulders and mild intellectual disabilities. It is caused by autosomal dominant mutations in the EYA1 gene in chromosome 8. Only 11 cases have been reported in medical literature. Otofaciocervical syndrome type 2
It is characterized by the same symptoms in type 1, this disorder is different from type 1 because of its genetic cause and because of its additional features: thymus development alterations with T-cell immunodeficiency and recurrent infections which may turn fatal. It is caused by autosomal recessive mutations in the PAX1 gene in chromosome 20. Only 13 cases have been described in medical literature. == References ==