Given the central role of KCNN4 in phenotypic modulation and neointimal formation [7], [18] and the recently described role of NOX5 in human SMC proliferation and atherosclerosis [51], [52], we tested the hypothesis that NOX5 is required for transcriptional upregulation of KCNN4 through AP-1. The gene discussed is NOX5; the disease is atherosclerosis.