The underlying pathophysiological mechanism of GPA-related DAH is linked to antibodies related to ANCA, which interact with inflammatory cells (neutrophils, monocytes, and lymphocytes) and cytokines (particularly Th1 cytokines, namely, tumor necrosis factor and interferon-γ) and then initiate and perpetuate vasculitis (68, 69). Here, TNF is linked to granulomatosis with polyangiitis.