It is hypothesized that infection with A. cantonensis activates the TLR4/MyD88 signaling pathway through Cav-1 phosphorylation, leading to increased activity of the NF-kB or MAPK/ERK/AP-1 signaling pathway, subsequently increasing MMP-9 activity, resulting in damage to the BBB, increased permeability, and inflammatory responses. This evidence concerns the gene MYD88 and infection.