USP30 and neoplasm: 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.