It is postulated that the VHL independent activation of other signal transduction pathways such as the mammalian target of rapamycin (mTOR), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), signal transducer and activator of transcription 3 (STAT-3), or epidermal growth factor receptor (EGFR) pathways could be responsible for tumour progression and tumours activated by several different mechanisms could be more aggressive [42]. Here, NFKB1 is linked to neoplasm.