Perforin is expressed in the granules of T-cells and NK-cells, and creates pores in the cytoplasm of targeted cells, thereby allowing granzymes and proteases to enter cells and ultimately induce apoptosis after entering the cell nucleus [1]; however, the perforin gene mutation may not lead to the development of the clinical features of FHL until a patient comes into contact with viral infectious agents and environmental agents [12,15]. This evidence concerns the gene PRF1 and hemophagocytic syndrome.