Given the established role of gut-derived lipopolysaccharide and TLR4 activation in CCM lesion formation, future research could apply FMT in CCM murine models to directly assess whether transferring dysbiotic microbiota from CCM patients induces or exacerbates lesion development, providing critical insights into the causal role of the gut microbiome in CCM pathogenesis. This evidence concerns the gene TLR4 and cerebral cavernous malformation.