LIF and hepatocellular carcinoma: In addition, ectopic LIF overexpression in HCC cells reversed the CVB‐D‐induced phosphorylation of p38MAPK at the Thr180/ Tyr182 sites (Figure 5A) and reversed the anti‐tumor effect of CVB‐D (Figure 5A,B and Figure S5B), demonstrating that LIF is a potential druggable target of CVB‐D.