Although AMPK activation is also documented to suppress the expression of bile acid transporters in hepatocytes and further be responsible for estrogen-induced cholestasis, which may result from the sustained over-activation of AMPK (Li et al., 2017), loss of AMPK promotes steatosis development in mice without affecting normal physiological functions (Boudaba et al., 2018; Zhao et al., 2020). This evidence concerns the gene PRKAA1 and cholestasis.