It increased the activity of DNMT3A, FOS, HMOX1, IL1B, IL6, JUN, and TNF. This implicates potential involvement of biological pathways associated with AHR pathway, apoptosis, chemical carcinogenesis, ferroptosis, fluid shear stress & atherosclerosis, oxidative stress response, and SUMOylation (Fig. 3). The gene discussed is JUN; the disease is atherosclerosis.