PRKN and neoplasm: identified that endogenous ARIH1 expression in lung cancer, breast cancer, and cervical cancer cell lines promotes the removal of damaged mitochondria via mitophagy, challenging the notion that the primary regulators of mitophagy are tumor suppressors.[14] KEGG enrichment analysis of DEGs between bulk RNA‐seq data for ARIH1‐overexpressing cells and control cells revealed that ARIH1, which is also a member of the RBR E3 ubiquitin ligase family, is associated with OXPHOS.