CCT6A promotes metastasis in liver cancer via metabolic reprogramming mediated by RPS3 [35], drives LUAD progression through the STAT1/HK2/glucose metabolism axis [36], enhances stemness in oral cancer via activation of the Wnt/Notch pathway [37], and activates the PI3K/AKT signaling pathway to promote epithelial–mesenchymal transition (EMT) and proliferation in breast cancer [38]. The gene discussed is STAT1; the disease is lip and oral cavity carcinoma.