Indeed, in spite of the protective function addressed by IL-23 against bacterial, fungal, and viral infections, extensive knowledge sustains the contribution of its alteration in triggering chronic inflammation and autoimmunity, providing a solid substrate for the development of several autoimmune diseases, like psoriasis, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), and multiple sclerosis (MS) [8,11,23,24]. This evidence concerns the gene IL23A and myeloid sarcoma.