Growth delay of tumor cells following knockdown of NOX1 expression appears to be due to a profound block at the G1/S transition of the cell cycle that is related to cyclin D1 down-regulation, and alterations in other components of the G1 checkpoint that may reflect a protein phosphatase-mediated inactivation of the mitogen-activated protein kinase (MAPK) pathway. This evidence concerns the gene NOX1 and neoplasm.