Asynchronous hemodynamics increased the mRNA levels of three atheroprotective genes: SCARB-1, which is a cell-surface HDL receptor that mediates HDL cholesterol efflux reducing atherosclerosis progression [39]; SOD-1 is one of three superoxide dismutases that destroys free superoxide radicals and whose overexpression inhibits angiotensin II-induced expression of MCP1 and monocyte infiltration [40]. The gene discussed is SOD1; the disease is atherosclerosis.