Recently, it has been shown that β-arr1 contributes also to endothelial dysfunction promoted by nicotine, by promoting its recruitment to the E-selectin promoter as well as E-selectin expression, thus facilitating adhesion of monocytes to EC and endothelial damage, revealing a novel role for nuclear β-arr1 in the growth and metastasis of NSCLC [43]. This evidence concerns the gene SELE and endothelial dysfunction.