Thus, in an environment such as hyperhomocysteinemia, where the level of homocysteine is disproportionally higher than normal, in addition to binding to all available PPARγ jeopardizing the normal ROS scavenging mechanisms, there is still enough homocysteine in the systemic circulation to promote oxidizing conditions within the cells due to the amount of auto-oxidation of homocysteine thiol groups. The gene discussed is PPARG; the disease is hyperhomocysteinemia.