The UV‐DDB complex, including DDB1 (LoH: 10.4%) and DDB2 (LoH: 8.0%; Figure S4b), facilitates binding of XPC to UVR‐induced lesions, and experimental evidence suggests its knockdown increases tumorigenic potential (Roy et al., 2013) and reduces overall survival (Bommi et al., 2018) in various cancers. The gene discussed is XPC; the disease is cancer.