Transcription-replication collisions at the highly expressed GAP1 gene can contribute to the formation of adaptive CNVs through ODIRA by inducing DNA replication errors. When the transcription machinery encounters the replication fork, it can lead to replication stress and fork stalling. This stalling can trigger DNA replication errors, such as template switching, which is a key mechanism in ODIRA. In ODIRA, short inverted repeats near an origin of DNA replication enable template switching of the leading strand to the lagging strand, resulting in the formation of CNVs with an inverted middle copy. The high transcriptional activity at the GAP1 gene increases the likelihood of transcription-replication collisions, leading to an increased rate of DNA replication errors and subsequent CNV formation through ODIRA. Therefore, the transcription-replication collisions at the highly expressed GAP1 gene can be a driving force behind the generation of adaptive CNVs through ODIRA.