In the hyperlipidemia model, with the disruption of the PCSK9/LDL receptor regulation axis caused by the dark and light cycle disorder and the liver BMAL1 rhythm gene disorder, the overexpression of TRIB1 restored the plasma PCSK9 level, increased the expression of LDL receptor protein, and restored plasma cholesterol homeostasis in mice lacking the liver clock gene 81. Here, LDLR is linked to hyperlipidemia.