In addition, complexes between constitutively active RON splice variants and β-catenin also interact with HIF1α to regulate HIF-1-dependent transcription and tumour cell proliferation under hypoxic conditions, confirming a close relationship between hypoxia-induced alternative RON splicing, β-catenin and HIF-target genes in the regulation of autonomous tumour cell growth and tumour progression (Fig. 2a) [99, 105–111]. The gene discussed is HIF1A; the disease is neoplasm.