Hence, while this and previous (16, 18) reports demonstrate the fundamental role of PI3Kβ and PI3Kδ in the pathogenesis of skin inflammation in EBA, our data presented here does not rule out that other class I PI3K isoforms contribute to EBA pathogenesis—especially PI3Kα, one PI3Ki selective for this isoform (alpelisib) impaired induction of experimental EBA. This evidence concerns the gene PIK3CD and acquired epidermolysis bullosa.