For example, tumour-associated inflammation may be induced by both KSHV and Pg through the NFkB pathway, sustained proliferation by KSHV, Pg, Td, and Fn through the Wnt, MAPK and PI3K-AKT pathways, activating tumour invasion by EBV and Pg through EMT, suppression of apoptosis by KSHV and Pg via p53 inactivation, genomic instability by KSHV and Aa through ATM, and immune evasion by KSHV, Td, and Aa through various pathways [60]. This evidence concerns the gene NFKB1 and neoplasm.