In summary, our observations show that, through HIF1A protein stabilisation and transcriptional activation (Fig8B), nuclear ARRB1 induces metabolic re-programming of prostate cancer cells which drives the expression of tumour-specific phenotypes, such as anchorage-independent growth, migration, invasion and proliferation, and confers on the cells a selective growth advantage that may promote tumour progression. This evidence concerns the gene HIF1A and neoplasm.