MYC and Burkitt lymphoma: MiR-92a, overexpressed in our series of PMBL human samples and Karpas cell line, can exert antagonist biological functions in experimental conditions: in the Eμ-myc Burkitt’s lymphoma model, it promotes c-Myc-induced apoptosis [19, 38]; in mouse embryonic fibroblasts, and in primary B-cells, it enhances c-Myc-induced cell proliferation [38].