In sharp contrast to existing strategies for tumor specific gene expression, which usually take advantage of aberrant promoter activation (hTERT [29], AFP [30]), hypoxic conditions in the tumor-microenvironment (HRE [31]) or tissue-of-origin-specific gene expression patterns (PSA [32]), our design relies on the unique and aberrant activity of tumor-defining fusion oncogenes, rather than the physiological action of non-mutated, but aberrantly expressed transcription factors. Here, AFP is linked to neoplasm.