The mechanism of hypercytokine storm from HLH resembling macrophage activation syndrome infers that the absence of BTK can augment inflammation cytokines through Toll-like receptor signaling pathways (TLR4, 7, 8, and 9) (37–39), possibly driving to the HLH process as two brothers in a previous report (40). This evidence concerns the gene BTK and hemophagocytic syndrome.