Sarcoidosis is a complex disease characterised by the presence of epithelioid non-caseating granulomatous inflammation affecting multiple organs and whose aetiology has been related to microbial, environmental and genetic factors [1, 2]. However, no single antigenic trigger has been identified, although associations with Propionibacterium acnes and mycobacteria pathogen-associated molecular pattern, deposition of serum amyloid A, and exposure to inorganic particles and insecticides have been suggested [3–5]. Occurrence of familial cases suggests that genetic variation contributes to disease pathogenesis with a heritability of about 39% [6]. Despite intensive genome-wide association studies, no single nucleotide polymorphism is, as yet, able to explain the “missing heritability” in the disease, especially for non-resolving, non-Löfgren syndrome sarcoidosis [5–7].