As leptin/lepR signaling has previously been implicated in intracellular ROS maintenance (Bilbao et al., 2015; Frühbeck et al., 2017), and one previous study in adipose tissues of T2DM mice reported that restoration of canonical leptin/lepR signaling attenuated intracellular ROS accumulation (Frühbeck et al., 2017), it is certainly possible the leptin resistance-UCP2-ROS signaling pathway might be associated with CVP neuronal dysfunction in T2DM. This evidence concerns the gene LEPR and type 2 diabetes mellitus.