This activation of MyD88 leads to the dephosphorylation of the nuclear factor kappa-B kinase subunit β [IKKβ], which cleaves the p65 peptide of the NFĸB complex, causing it to translocate to the nucleus, where it acts as a transcription factor for increases in the expression of IL-6 and Calcineurin B. IL-6 induces VEGF, which in turn increases angiogenesis and vascularization, necessary mechanisms for nourishment of tumor cells [25]. The gene discussed is IKBKB; the disease is neoplasm.