These findings are in line with previous research stating the key function of CD4+ cells [46] and dysregulation of Janus kinase–signal transducer and activator of transcription (JAK/STAT) signalling in sarcoidosis [46, 47, 48], therefore providing a pathophysiological rationale for the possible application of JAK inhibition in SaM. The gene discussed is SOAT1; the disease is sarcoidosis.