Deficiency of the KRIT1 gene leads to instability of integrin cytoplasmic domain‐associated protein‐1 (ICAP1), which promotes the activation of β1 integrin, resulting in increased ras homolog family member A (RhoA)–dependent contraction of the extracellular matrix and destabilization of intercellular junctions, thus contributing to the progression of CCM lesions (W. Liu et al. This evidence concerns the gene RHOA and cerebral cavernous malformation.