More recently, a comprehensive analysis using spectral flow cytometry provided novel insights into the expression patterns of key inhibitory and stimulatory immune molecules on B-cells in GPA, suggesting that changes in the expression of molecules such as FcγRIIB, CD21, CD86, and CD22 on specific B-cell populations, combined with the strong association of FcγRIIB, BTLA, and CD21 expression with disease activity, reveal the complexity of immune regulation in the pathogenesis of GPA [37]. Here, FCGR2B is linked to granulomatosis with polyangiitis.