Tumour promoting subversion of pre-mRNA splicing by hypoxia, resulting in oncogene activation, tumour suppressor inactivation, immortalization, metabolic adaptation, evasion of programmed cell death and anti-tumour immunity, angiogenesis, tumour-promoting inflammation and genetic instability, not only depends upon specific alternatively spliced protein isoforms but also specific spliceosome components, splicing factors, splice factor kinases and splicing, all of which represent potential therapeutic targets. This evidence concerns the gene SLU7 and neoplasm.