The B‐cell non‐Hodgkin lymphomas (B‐NHL) are a diverse group of haematological malignancies which arise from the mature B‐lymphocyte compartment. Recently, our understanding of the molecular pathogenesis of these disorders has greatly increased due to technological advances such as high‐throughput DNA sequencing techniques. A paradigm of B‐NHL pathogenesis has emerged where the normal genetic processes that are central to generating B‐cell receptor diversity (somatic hypermutation and class switch/VDJ recombination) also drive the genesis of large‐scale, chromosomal‐level genetic lesions and smaller‐scale gene‐level mutations to produce the malignant phenotypes observed. Whilst a significant degree of genetic heterogeneity exists within each B‐NHL subtype, the genetic lesions present within each subtype show a degree of convergence on common intracellular signalling, epigenetic and cell cycle pathways. This convergence gives an insight into the key oncogenic drivers of specific B‐NHL subtypes and potential targets for therapeutic intervention. This review covers the current understanding of the causative genetic processes of B‐NHL, the associated driving molecular lesions and the implications of these findings for the treatment of this group of disorders.