Therefore, the downregulation suggests a protective role of normal EVs, which appears to be absent in those isolated from preeclamptic placenta.[54] This, however, is in contrast with another study that reported an upregulation of ICAM‐1 after uptake of preeclampsia‐derived EVs by human dermal microvascular endothelial cell‐1 (HMEC‐1).[55] The difference in ICAM‐1 levels may be due to the variation in recipient cell types, but may also be a result of a different internalization route. This evidence concerns the gene ICAM1 and preeclampsia.