[2] Gag genes are part of a general architecture for retroviruses, viruses that replicate through reverse transcription, where the gag region of the genome encodes proteins that constitute the matrix, capsid and nucleocapsid of the mature virus particles.
Due to evidence[5] 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.
[6] 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.
In the case of the murine leukemia viruses, a species of viruses capable of causing cancer in murines (mice), the viral life cycle can also be responsible for oncogenesis through a Gag-v-Onc fusion protein called "Mo-MuLV(src)", which is a Gag-v-Src protein capable of inducing oncogenesis in living mice.