We also found that AGK2 treatment enhanced the ubiquitination of FGL1 in a dose-dependent manner (Figure 2J) and decreased FGL1 protein levels in multiple HCC cell lines, as measured by both immunoblotting and ELISA (Figure 2K and Supplemental Figure 2, C–E), while the FGL1K98R mutant was resistant to AGK2-induced degradation (Figure 2L). Here, FGL1 is linked to hepatocellular carcinoma.