Emerging data suggest that palms and soles are predisposed to pustular inflammation in PPP because dense eccrine ducts leak IL-1–rich sweat through tight-junction gaps weakened by reduced claudin-1, while frictional stress activates Piezo-1 channels, amplifying IL-36 and IL-1β in keratinocytes that already express high IL-36, S100A8/A9 and type-I interferons. Here, IL1B is linked to palmoplantar pustulosis.