Cxs have been characterized as tumor suppressors in the past, with the main evidence thereof being as follows: (1) Tumor cells lack functional GJIC, and cancer cells do not express Cxs in HeLa28 [18] and MCF-7 cancer cells [19]; (2) Tumor-promoting chemicals and conditions reversibly inhibit GJIC; (3) Some oncogenes, including src, ras, raf, and mos, can decrease the expression of GJIC; (4) Cx gene transfection inhibits the growth and decreases the tumorigenicity of tumor cells [19, 20]; (5) Mice with connexin-32 knockout can develop spontaneous and chemically induced liver cancer [20]. The gene discussed is MOS; the disease is cancer.