Perhaps more importantly, we verified the physiological relevance of the in vitro capacity of metformin to inhibit the demethylase activity of KDM6A/UTX by assessing its capacity to promote H3K27me3 methylation in animals and in human‐derived samples when used at therapeutic dosages commonly employed to treat T2D, as a surrogate of metformin‐induced changes in KDM6A/UTX activity in vivo. Here, MBD2 is linked to type 2 diabetes mellitus.