Also, in tumor-bearing mice models, researchers found that propofol activated tumor-associated macrophages (TAMs) were able to secrete microvesicles (MVs), which delivered extrinsic miR-142-3p to HCC cells, thereby down-regulating ras-related C3 botulinum toxin substrate 1(RAC1) expression and inhibiting HCC invasion (41). The gene discussed is RAC1; the disease is neoplasm.