Insulin resistance has been assigned a pivotal role in the pathological progression associated with type 2 diabetes and other chronic metabolic diseases. However, the molecular mechanism involved in this progression is still incompletely understood, and there are still no effective approaches to scavenge it. Many biological molecules, such as ROS, IRS-1, PI3K, have been identified involving in the causes of insulin resistance. Restoring these molecules could ameliorate the phenomenon of insulin resistance. BVR was known for a long time solely as an enzyme reducing biliverdin to bilirubin in the heme metabolic pathway. Presently, accumulative research data showed that BVR was a strong antioxidant enzyme, which could scavenge the excess ROS, and the characteristics of kinase activity and binding with p85 could modulate the biological function of IRS-1 and PI3K. We hypothesize that BVR has a significant role in the progression of insulin resistance, and it will be a promising therapeutic target for treating insulin resistance.