One plausible mechanism, not currently investigated could involve the decrease of oxidative stress within the plaque microenvironment by the 17-βE solution, 17-βE loaded CREKA-peptide modified nanoemulsion system and blank CREKA-peptide modified nanoemulsion, through downregulation of Nox1 and Nox4 NADPH oxidases that are known for their role in the progression of atherosclerosis in ApoE-/- mice.[52, 53]. The gene discussed is NOX1; the disease is atherosclerosis.