According to Giamarellos-Bourboulis, the hypothesis for a role of S. aureus skin colonization in HS flare-ups is supported by (i) the attenuated ability of phagocytosis of S. aureus by macrophages (in which the phagocytic capacity is inhibited by overproduction of interleukin (IL)-26 in HS); (ii) the greater production of human β-defensin–2 (hBD-2) by whole blood stimulated with heat-killed S. aureus in HS patients compared with healthy control subjects [53]. The gene discussed is IL26; the disease is histiocytic sarcoma.