As Rab22 and Rac1 are activated by Arf6 (Fig. 3, Fig. 5g), and they direct the traffic of junction proteins to cell-cell contact sites via mutual signal crosstalk [21], it is most likely that Arf6 intervention changed the selective targeting of CD147 and the retention of ZO-1 and E-cadherin to lateral membranes (Fig. 4g-j), which cooperatively triggered the disassembly of functional junctions between adjacent liver cancer cells. The gene discussed is ARF6; the disease is liver cancer.