In line with the observations reported above, the abrogation of CLU expression in mouse models of neuroblastoma, prostate, lung, and skin carcinogenesis leads to a quicker progression of the neoplasia toward the invasive phenotype [140,141,142,143], while targeting CLU with siRNA or antisense oligonucleotides enhances the cytotoxicity of chemotherapeutic drugs, ionizing radiation, and hormonal therapy [144,145]. The gene discussed is CLU; the disease is neoplasm.