The clinical outcome of sarcoidosis (SA) is very similar to tuberculosis (TB); however, they are treated differently and should not be confused. In search for their biomarkers, we have previously revealed changes in the phagocytic activity of monocytes in sarcoidosis and tuberculosis. On these monocytes we found a higher expression of receptors for the Fc fragment of immunoglobulin G (FcγR) in SA and TB patients vs. healthy controls. FcγRs are responsible for the binding of immune complexes (ICs) to initiate an (auto)immune response and for ICs clearance. Surprisingly, our SA patients had a high blood level of ICs, despite the abundant presence of FcγRs. It pointed to FcγR disfunction, presumably caused by the polymorphism of their (FCGR)genes. Therefore, we present here an analysis of the occurrence ofFCGR2A,FCGR2B,FCGR2C,FCGR3AandFCGR3Bvariants in Caucasian SA and TB patients, and healthy individuals with the use of polymerase chain reaction (PCR) and real-time PCR. The presented data point to a possibility of supporting the differential diagnosis of SA and TB by analyzingFCGR2C,FCGR3AandFCGR3Bpolymorphism, while for severe stages of SA also by studyingFCGR2Avariants. Additionally, the genotyping ofFCGR2AandFCGR3Bmight serve as a marker of SA progression.