Our working hypothesis is that the observed increased surface levels of CD44, as well as the deregulated expression of other genes from our RNA-seq dataset with reported involvement in biological processes related to cell adhesion and migration (such as LGALS3, CCL22, CD52, CROCC, and CTTLL3), might promote a more aggressive lymphoma cell phenotype and result in more disseminated malignancy. This evidence concerns the gene CCL22 and lymphoma.