These results mirror our recent demonstration of the effects of stable NOX1 knockdown with shRNA in HT-29 cells [16]; in those experiments, we found that inhibition of NOX1 expression (and consequently of ROS formation) in the HT-29 line produced a profound block in cell cycle progression at the G1 interface (related to diminished cyclin D1 expression), leading to a significant decrease in tumor cell proliferation. This evidence concerns the gene NOX1 and neoplasm.