Furthermore, skin explants of pustular psoriasis cultured with a neutralizing anti-IL-26 mAb but not anti-IL-17A mAb completely inhibited the expression of CXCL1, CXCL8, and IL1A (Fig. 3 F), confirming the specific role of IL-26 as a driver of pathogenic autoinflammation circuits. Here, IL26 is linked to pustular psoriasis.