HCK and cutaneous vasculitis: Heterozygous gain-of-function mutations in HCK resulted in increased kinase activity of HCK and enhanced activation of myeloid cells, including migration and production of inflammatory cytokines [IL-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α] resulting in an autoinflammatory disorder characterized by cutaneous vasculitis and interstitial lung disease.59