LAUSR

responses in HS. However, the multitude of pathways affected by its inhibition strongly suggests that, in contrast to other IL-17-driven diseases such as psoriasis, the inflammatory response in HS is much broader, as is increasingly recognized. Even though most translational investigations have focused on IL-17A, significant overproduction of other IL-17 isoforms (e.g. IL-17C and IL-17F) is observed in HS tissue, and this may contribute to disease activity. Interestingly, heteromeric isoforms with IL-17RA can bind both IL-17A and IL-17C, thus reaching further than secukinumab, which targets IL-17A, whereas bimekizumab inhibits IL-17A, IL17F and IL-17AF. In conclusion, this study by Navrazhina and colleagues offers both mechanistic insights and biomarker candidates to better characterize the molecular response to IL-17RA inhibition. Moreover, their study provides directly applicable strategies to dissect inflammatory patterns in patients with HS as a prerequisite for a precision medicine-driven approach.