Under the condition of starvation, TFEB is phosphorylated by ERK and translocated into the nucleus, and eventually activates autophagy.7 TFEB has also been linked to lipid metabolism and oxidative stress in hepatocytes,32, 36 both of which are crucial factors in the development of liver diseases, including NASH.37 Therefore, pharmacological activation of TFEB represents a rational approach. This evidence concerns the gene TFEB and liver disorder.