Is this mechanism of action applicable in CLE as well? We

believe, yes, that this mechanism of action is definitely applicable.

in CLE, when we look at the histopathology of CLE versus cutaneous lesions in SLE, they look identical.

And thus, you know, the notion here is that a therapy such as anaphylumab, which specifically targets this pathway at the level of the receptor, would also be effective in lesions of CLE.

And in fact, anaphylumab has been a game changer in the treatment of cutaneous lupus in the setting of SLE, for which it is approved.

And what's been so striking about this therapy, in my experience, and what the literature has shown us, right, Vicki, is that this mechanism acts quickly and we see resolution of inflammation in the skin faster than we've seen with our other targeted therapies.

And I think this is really a proof of concept of the critical role importance of type 1 interferon in the pathogenesis of skin lesions, the fact that we can block the type 1 interferon receptor and see such a dramatic response has been quite striking and has been very helpful for our patients living with SLE with cutaneous manifestations.

So, lidofilumab is an investigational BDCA2-directed therapy, and how does its mechanism of action differ from standard approaches for treating CLE?