Results from further cellular experiments, as well as analysis of a nude mouse xenograft model, revealed that SPR depletion inhibited HCC cell proliferation and promoted apoptosis, affirming that SPR may regulate hepatocellular carcinoma progression via the FoxO3a/Bim pathway (a transcriptional target in apoptosis regulation in vivo and in vitro) (99). Here, BCL2L11 is linked to hepatocellular carcinoma.