SOAT1 and toxic epidermal necrolysis: Using a new autologous co-cell culture of PBMCs from TEN survivors and healthy KCs, JAKi efficiently blocked TEN survivor-derived PBMC-driven KC cell death (Fig. 1b).1 This finding led the authors to demonstrate the involvement of JAK-STAT signaling in two mouse models of TEN: In their first model, subcutaneous injection of smac (second mitochondria-derived activator of caspases) mimetics resulted in cutaneous inflammation and epidermal detachment, as seen in TEN.