Background
Genes that have been subject to adaptive evolution can produce varying degrees of pathology or differing symptomatology. ErbB family receptor activation will initiate a number of downstream signaling pathways, such as mitogen-activated protein kinase (MAPK), activator of transcription (STAT), the modulation of calcium channels, and so on, all of which lead to aggressive tumor behavior. However, the evolutionary mechanisms operating in the retention of ErbB family genes and the changes in selection pressures are not clear.