As shown in Figure 6C,F,I, regardless of SLC1A5, SLC38A2, or their combined siRNA-mediated inhibition, Huh7 and Hep3B HCC cells maintained their capacity to utilize exogenous glutamine for the optimization of cell survival in a dose-dependent manner (Huh7: all p < 0.05; Hep3B: SLC1A5 siRNA: p < 0.001, SLC38A2 and combined siRNA: both p < 0.01). This evidence concerns the gene SLC38A2 and hepatocellular carcinoma.