The differences between DIO and T1D regarding the pathways associated with inflammatory responses (TREM1, PRR, MAPK, HMGB1, STAT3, Th1/Th2, and MSP-RON) and oxidative stress (production of NO and ROS, the antioxidant action of vitamin C) might be responsible for enhanced lung toxicity of PM exposure in T1D mice. This evidence concerns the gene HMGB1 and type 1 diabetes mellitus.