PDCD10 and cerebral cavernous malformation: In contrast, CCM3–/–CI‐huVEC clones proliferated well to high passages and had slightly lower SA‐β‐gal activities under serum starvation which is in agreement with observations from CCM3‐silenced primary human coronary artery ECs after replicative stress.46 Taken together, these results suggest that clonal expansion of mutant ECs contributes to CCM pathobiology.47