For example, genetic ablation or pharmacological inhibition of the K3K9me2-specific demethylase KDM3a was shown to diminish collagen deposition in the mouse TAC model (142), and myofibroblast-specific ablation of lysine-specific demethylase 1 (LSD1/KDM1) was found to alleviate systolic dysfunction and fibrosis in the TAC model by broadly interdicting pathological TGF-β1 signaling (143). Here, KDM3A is linked to persistent truncus arteriosus.