The activation of mononuclear system cells occurs due to a hypersecretion of proinflammatory cytokines (IFNγ, TNFα, IL6, IL10, M-CSF), as a consequence of a triggering agent, which is often a viral infection [11] . The underlying problem is a T and Natural Killers cells dysfunction, which leads to an uncontrolled immunological response [12] due to inability to eliminate the triggering agent. All viral, bacterial, parasitic and fungal cultures performed in our case were negative. Impaired perforine function due to gene mutations seems to play an important role in HFS pathogenesis, as reported in literature [12] . They are implicated in cytotoxicity by forming a death-inducing pore in target cell [13] .