The present findings provide compelling evidence to support a protective role of DCHT in ANIT-induced intrahepatic cholestasis with liver injury, as demonstrated by the changes of gallbladder and liver histopathological morphology, aforementioned enzymatic indicators, the phosphorylation of p38 MAP kinase, the dephosphorylation of ERK1/2, as well as an increase in the proapoptotic/antiapoptotic (Bax/Bcl-2) ratio in the liver tissue. This evidence concerns the gene STK39 and intrahepatic cholestasis.