We previously reported that highly aggressive GBC-SD cells overexpressed EphA2, FAK and Paxillin-P formed in vitro and in vivo VM networks through the activation of the EphA2/FAK/Paxillin signaling pathway; and TIMP-2 effectively inhibited expression of these VM signaling-related markers, i.e., the EphA2/FAK/Paxillin signaling pathway, thus inhibiting VM of GBC-SD cells in vitro and in vivo[42]. The gene discussed is EPHA2; the disease is Salla disease.