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Figure 2. Schema showing the partial list of miRs involved in neuroblastoma (NB) therapy resistance. While MYCN regulated miRs have been documented to play crucial role in the therapy resistance through orchestrated clonal expansion and defying differentiation, acquired modulation of upstream miRs those regulate MYCN also plays crucial role in coordinating drug resistance and disease evolution. Hypermethylation of tumor suppressor miRs and hypomethylation of oncomiRs with clinical therapy in surviving cancer cells is regarded as one of the major mechanism for acquired loss of TS miRs and gain of oncomiRs, those dictate drug-resistance. Rearrangements on the levels of many key miRs inflicting therapy resistance through unique signaling flow-through are documented. Conversely, regulation/deregulation of many miRs converge on a signaling or functional event (e.g., Bcl2) to effect resistance. It is clearly evident that miRs play definitive roles in therapy resistance and miR-targeted approach could be an effective strategy for the treatment of resistant NB