Previously, ACTB, in head and neck squamous carcinoma (HNSCC) and other cancers, was found to impact tumor metastasis as well as tumor invasion through NF-κB and Wnt-β-catenin protein pathways (Frontelo et al., 1998; Rubie et al., 2005; Popow et al., 2006); Wright A et al. reported that CYLD could limit the persistent activation of NF-κB signaling by deubiquitinating RIPK1, thus activating necroptosis-related pathways (Wright et al., 2007; Gong et al., 2019). Here, RIPK1 is linked to neoplasm.