Overexpressing a stabilized form of USP30 promoted tumor growth in DEN/CCl4-induced HCC, whereas USP30 knockout reduced tumorigenesis in mice.423 Furthermore, it has been shown that mitophagy is suppressed during T cell exhaustion; knockout of USP30 or inhibition of USP30 by the specific inhibitor ST-539424 rejuvenates effector function in exhausted CD8+ T cells, enhancing their antitumor immunity.305 Together, these findings provide proof of concept that USP30 inhibition may be exploited not only for neurodegenerative disorders but also for cancer therapy. This evidence concerns the gene CD8A and neoplasm.