Interestingly, we observed increased viability and invasion in Hep3B and Huh7 cells upon RNase1 treatment, which could be repressed by pretreatment with crizotinib or Alectinib (Supplementary Fig. 7h–j), suggesting that ALK is also essential for the biological activities of RNase1 in HCC tumor cells. Here, ALK is linked to neoplasm.