RAC1 and endometriosis: Wu et al. demonstrated that eutopic and ectopic endometrial stromal cells from patients with endometriosis exhibit higher VCL expression, increased actin polymerization, elevated levels of small GTPases (predominantly ras homolog family member A (RHOA), but also ras-related C3 botulinum toxin substrate 1 (RAC1) and cell division cycle 42 (CDC42)), and enhanced migratory abilities compared to endometrial stromal cells from women without endometriosis.