To investigate whether the PKC-dependent nucleocytoplasmic shuttling of KRIT1 observed in HeLa cells could be recapitulated in an endothelial cellular model, which is more closely related to CCM disease, we tested the effects of PMA and BIM+PMA treatments on primary human pulmonary artery endothelial cells (HPAECs) transiently transduced with adenoviral mCherry–KRIT1. Here, PRRT2 is linked to cerebral cavernous malformation.