Fig. 5.

Schematic view of apoptotic pathways in vitiliginous keratinocytes. Tumor necrosis factor (TNF)-α is supposed to activate phosphatidylinositol 3-phosphate (PI3K)/apoptosis signal-regulating kinase (AKT), which, in turn, activates nuclear factor (NF)-κB through sequential activation of Iκβ kinases (IKKs) and inhibitor-κB (I-κB), resulting in inhibiting apoptosis. However, activation of AKT and NF-κB was reduced in depigmented epidermis, whereas the Fas/Fas-ligand (FasL) pathway was normal. FLIP: FLICE (fas-associated death domain protein-like interleukin-1-beta-converting enzyme)-like inhibitory proteins.