To date, the genetic program that regulates the mechanisms by which E. granulosus infection occurs and induces liver pathology is largely unknown, although the liver is most fre-quent location of echinococcal cysts in the liver, representing approximately 70% of cases echi-nococcal cysts [2,3]. In turn, studies on the molecular mechanism of host response to AE caused by infection with E. multilocularis have been well documented in the hepatic transcrip-tome level [21–23], and furthermore, the nuclear genomes of E. multilocularis and E. granulo-sus have already been characterized recently [24,25], which may help gaining a deeper understanding of host-parasite interaction