FLNA and arterial disorder: Furthermore, Hitomi et al. reported that p.R4810K induced a mitotic abnormality and genome instability by the functional inhibition of the metaphase–anaphase spindle checkpoint protein mitotic arrest deficiency 2.[47] More recently, it was reported that RNF213 targeted filamin A and nuclear factor of activated T cells for proteasomal degradation, attenuating the non-canonical Wnt/calcineurin pathway,[48] which plays a key role in angiogenesis and cardiac development.[49] Further analyses will shed light on the molecular link between intracranial and extracranial arterial diseases.