The Gag-v-Onc fusion protein from the Rous sarcoma virus illustrates the dual role that the fusion protein plays in the viral and host cellular life cycle. For example, the viral gene Src (as in "sarcoma") is not necessary for viral reproduction, but does affect virulence. Due to evidence of conserved homology between the v-Src gene and its host (animal) genomes, and its non-essential status for viral reproduction, the v-Src gene is likely to have been acquired from a host genome and altered by subsequent mutations. These subsequent mutations are responsible for the oncogenic capabilities of the virus, as the normal (host) version of the Src gene, c-Src promotes survival, angiogenesis, proliferation and invasion pathways. These native pathways are disrupted in the presence of the mutant Src gene (v-Src) such that oncogenesis becomes more likely for the infected host cells, since the v-Src gene is translated into a functionally distinct version of its host counterpart.