An inflammatory situation was created by stimulating the endothelial cells and the trophoblasts with TNF-α, an inflammatory cytokine expressed by these cells during preeclampsia, and the authors saw that the concentration of FKBPL and Gal-3 increased in the microfluidic device compared to that measured in a non-inflammatory condition and that the trophoblasts were responsible for the observed reduced formation of the placental vascular network [126]. This evidence concerns the gene LGALS3 and preeclampsia.