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谢谢大家！ Stein Figure 2 (Harris et al). Events in B-cell receptor gene rearrangement. Schematic representation of the immunoglobulin gene rearrangement and of the resulting protein. Abbreviations: V, Variability segment; D, Diversity segment; J, Joining segment; C, Constant region; N(N’), hypervariable regions of variable length and composition.  Stein Figure 3 (Harris et al). Somatic VH mutations. This process introduces point mutations and occasional deletions and duplications, especially into the heavy- and light-chain variable-region genes. CH and CL denote the gene segements encoding the constant regions of the heavy and light chains, respectively.  Stein Figure 4 (Harris et al). Receptor editing. Receptor editing modifies the genes encoding the Ig molecules by a process in which an originally rearranged Ig segment, usually the light chain, is replaced by another one. The new light chain gene is generated by a secondary rearrangement of the variable region gene in the light chain loci.  Figure 5. Model of B-cell non-Hodgkins lymphoma (NHL) histogenesis and pathogenesis. A lymphoid follicle, constituted by the germinal center (GC) and the mantle zone (MZ), is represented together with the surrounding marginal zone (MargZ). Based on the absence or presence of IgV somatic mutations, B-cell NHL can be distinguished into two broad histogenetic categories: i) pre-GC derived NHL, lacking IgV mutations and including mantle cell lymphoma (MCL); ii) B-cell NHL derived from a cell that transited through the GC and harboring mutated IgV genes, exemplified in the figure by follicular lymphoma (FL), lymphoplasmacytic lymphoma (LPL), MALT lymphoma, diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma (BL). In B-cell chronic lymphocytic leukemia/ small lymphocytic lymphoma (CLL/SLL), the presence of somatically mutated IgV genes in 50% of the cases also suggests a derivation from a GC experienced B cell.49 For each category, the arrow indicating the histogenet