Indeed, TNFAIP3 and NFKBIA mutations are more frequent in EBV-uninfected cHL, indicating that in EBV-positive cases, viral LMP1, as a strong NFκB activator, can replace the need to inactivate TNFAIP3 or NFKBIA [28,30]. Here, NFKB1 is linked to classic Hodgkin lymphoma.