To validate the bridging function of ATG5 to SH3BGRL-exerted tumor suppression, we approached the xenograft tumor formation and verified that the extra depletion of ATG5 remarkably counteracted the repressive role of SH3BGRL in tumorigenesis of HepG2 cells, compared to the SH3BGRL-overexpressing cells that induced no tumor formation at all (Figure 6(c)), confirming the mediator function of ATG5 in SH3BGRL-rendered tumor suppression. This evidence concerns the gene SH3BGRL and neoplasm.