Using experimental endometriosis models induced in wild-type and gal-1-deficient (LGALS1(−/−)) mice, researchers demonstrated that gal-1 regulates the formation of vascular networks in endometriotic lesions and contributes to the growth of their ectopic foci, independently of VEGF and plasmacytoid-derived CXC-motif (CXC-KC) chemokines [109]. Here, LGALS1 is linked to endometriosis.