The role of genetic factors for the lack of therapeutic response to anti-TNFα agents was previously suggested in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), juvenile idiopathic arthritis (JIA), and Sjögren’s syndrome, as well as in inflammatory bowel disease, in particular Crohn’s disease (CD), but also in Wegener’s granulomatosis and sarcoidosis [4,29,30,31,32,33,34,35,36,37,38,39,40]. Here, TNF is linked to granulomatosis with polyangiitis.