showed that endothelial Toll‐like receptor 4 (TLR4) stimulation by lipopolysaccharide derived from Gram‐negative gut bacteria is required to activate the MEKK3–KLF2/4 pathway and drive lesion formation in CCM mouse models: germ‐free mice or animals with genetic or pharmacologic blockade of TLR4 were protected from CCM development, whereas activation of TLR4 or polymorphisms increasing TLR4 or CD14 expression were associated with higher lesion burden in humans (Tang et al. 2017). The gene discussed is MAP3K3; the disease is cerebral cavernous malformation.