One study showed that overexpression of TEAD1 in skeletal muscle activates GSK3β and decreases nuclear levels of β-catenin and NFATc1/c3, which was reversed by mechanical overload 61 suggesting a potential link between TEAD1 and GSK3β in regulating AKI, however further studies are required to confirm this connection. Here, TEAD1 is linked to acute kidney injury.