Prompted by the notion that the membrane channels in gap junctions conduct growth-regulating signals from cell to cell, we transferred the α1 gene for the channel protein (connexin43) of rat heart to tumorigenic mouse MCA-10 cells. Upon incorporation into the cell genome, this exogenous gene was expressed, resulting in functional channels and normal growth regulation: cell—cell communication, determined with a channel-permeant 400-dalton fluorescent tracer, was increased and tumorigenicity, determined in nude mice, was suppressed.