In summary, as hypothesized in our working model of the role of NOX1-generated ROS in colon cancer growth (Fig. 10), we suggest that some human colon cancers, particularly those with high levels of NOX1 expression, require an oxidative selective pressure to maintain the level of genomic instability required for optimal proliferation, angiogenesis, and/or metastatic potential (9, 11). Here, NOX1 is linked to colonic neoplasm.