Here, we extend those studies in the following two ways: (1) we show that genetic silencing of KRIT1 triggers similar transcriptional programs to those initiated by HKi2, and (2) we show that under conditions of disturbed flow, known to trigger transcriptional changes associated with predisposition to atherosclerosis, silencing KRIT1 leads to a transcriptional program more like that observed in atheroprotective laminar flow. The gene discussed is KRIT1; the disease is atherosclerosis.