One possible mechanistic explanation is that lower expression of surface TIM-3 on immune cells during early-onset preeclampsia may allow cytotoxic T and NK cells to escape Gal-9-induced negative regulation, ultimately leading to uninhibited expansion of Th1 and Th17 response and to persistent inflammatory response usually seen during early-onset preeclampsia. This evidence concerns the gene LGALS9 and preeclampsia.