As another example, IL-10 function as an anti-inflammatory mediator, counteracting the production and activity of pro-inflammatory cytokines such as IL-1β and IL-6, which have been shown to favor PC progression and aggressiveness, has led to its development as a therapeutic agent; however, its double-edged activity as a suppressor of CD4 responses and DC maturation may possibly explain its therapeutic failure in recent clinical trials in PC. This evidence concerns the gene IL1B and pachyonychia congenita.