Although the exact pathogenesis of pembrolizumab-induced TEN is unclear, Goldinger et al suggest that PD-1 inhibitors disrupt the interaction of keratinocyte self-antigens and autoreactive CD8+ T-cell activity, which is crucial for T-cell homeostasis in preventing severe cutaneous drug reactions, suggesting that T cells, not keratinocyte-mediated factors or natural killer cells, are the drivers of this reaction.9 The gene discussed is CD8A; the disease is toxic epidermal necrolysis.