For example, hypoxic colorectal cancer cells shift the DDR pathway coding transcripts to non-coding intron-retained alternative spliced transcripts in the HDAC6 gene encoding histone deacetylase 6, which leads to impaired DNA double-strand break (DSB) repair and genomic instability, by modulating the inhibitory alternative splicing of the tumor suppressor p53-binding protein 1 (TP53BP1) and TP53 co-factor (Memon et al., 2016). This evidence concerns the gene TP53BP1 and colorectal cancer.