Abnormal expression of miR-135a has been documented in several cancer types, but the most striking evidence of the involvement of miR-135a in B-cell tumors was reported in Hodgkin’s lymphoma tumors, where Navarro et al.39 demonstrated the causal relationship that linked miR-135a to JAK2 downregulation and to the consequent disruption of STAT-mediated Bcl-xL anti-apoptotic function: low miR-135a level was significantly associated to higher proliferation rate and poorer outcome. This evidence concerns the gene SOAT1 and Hodgkins lymphoma.