So in LX2 cocultured induced sorafenib resistance in Huh7, LX2 secreted HGF into the tumor microenvironment which activated HGF/c-Met axis and thus activates p-Akt and then reactivated p-ERK somehow which finally led to the increased level of antiapoptotic protein and decreased caspase cleavage. The gene discussed is HGF; the disease is neoplasm.