In a meta-analysis of seven genome-wide association studies totaling 5325 HL cases and 22,423 control patients, integration of gene expression, histone modification, and in situ promoter capture Hi-C data at the five new and 13 known risk loci implicates the dysfunction of the germinal center reaction, disrupted T-cell differentiation and function and constitutive NFκB activation as mechanisms of predisposition [20]. This evidence concerns the gene NFKB1 and Hodgkins lymphoma.