In lung adenocarcinoma, overexpression of FGF4 promoted epithelial to mesenchymal transition of tumor cells by elevating store-operated calcium entry and expression of calcium signal-associated protein Orai1 aggravating cancer [159]; however, in breast cancer, the combinatory role of the oncoprotein hepatitis B X-interacting protein (HBXIP) and Sp1 transcription factor activated the FGF4 promoter, giving rise to FGF4 overexpression [162]. The gene discussed is LAMTOR5; the disease is breast cancer.