Non Hodgkin’s lymphoma (NHL) is a heterogeneous group of lymphoid neoplasms that arise mostly from different stages of B-cell development and account for approximately 90% of lymphoma cases. Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma (FL) are the most common types of NHL accounting for around 50% of cases. Advances in molecular and genomic approaches have discovered genes and pathways that can in part explain the high heterogeneity in morphology, tumour biology and clinical outcome. However, the high genetic heterogeneity observed within these NHL subtypes has limited the identification of genes and pathways with biological and clinical relevance, which in turn has limited the discovery of novel, target-specific and effective therapies that increase the survival rates of patients suffering from NHL. A recent study performed by the Griffith Lymphoma Project (GLP), using an integrative analytic approach of gene expression and copy number variation data from cases with DLBCL and FL, identified common genetic alterations across DLBCLs and FLs, targeting mainly the MAPK signalling pathway. These findings, apart from involving the MAPK signalling pathways as a crucial pathway in the lymphomagenesis of NHL, also unmasked the existence of common pathogenic mechanisms underlying the malignant phenotype of these B-cell lymphomas. These results also revealed that the investigation of common alterations in the mechanisms underlying the pathogenesis of these NHL subtypes is biologically and clinically relevant, as it provides a better understanding of the origin and progression of these lymphomas, and could unmask novel chemotherapeutic targets with a higher effectivity and selectivity than the available treatment for NHL.