Together with our findings that combined inhibition of MLKL-dependent necroptosis and caspase-8-dependent apoptosis fully prevented skin lesion development in ZBP1caE-het mice, these results showed that ZBP1ca caused skin inflammation by inducing RIPK3-MLKL-dependent necroptosis and to a lesser extent RIPK1-mediated caspase-8-dependent cell death in keratinocytes. Here, RIPK3 is linked to dermatitis.