The upregulation of cFos has been shown to cause apoptosis in a number of different cancers [76–83], in a mechanism that might involve activation of Fas ligand (FasL) transcription through the AP1 transcriptional activator consisting of the Fos/Jun heterodimer, which in turn promotes apoptosis through the FasL/Fas receptor pathway [76, 79–82]. This evidence concerns the gene FOS and cancer.