SLC7A7 and lysinuric protein intolerance: To the same extent, an increased production of cytokines by macrophages and epithelial cells upon SLC7A7 silencing could give reason of pulmonary complications in LPI: on the one hand, the spontaneous production of inflammatory cytokines by y+LAT1 defective epithelial cells may stimulate them in an autocrine activation; on the other hand, SLC7A7/y+LAT1 defect in both cell types could exacerbates lung inflammation in LPI through a macrophage-epithelial crosstalk.