In the context of bacterial sepsis or viral infection, it is possible that high levels of circulating LPS or viral proteins could continually engage TLR4 on the cell surface, activating MyD88-dependent signaling, while the rate-limiting step of endocytosis may lessen the extent of MyD88-independent signaling in comparison, shifting the balance towards a proinflammatory response consistent with cytokine storm. This evidence concerns the gene MYD88 and viral infectious disease.