These phenotypes were not observed in the same transfected cells systems, as could be explained by the differences in inhibiting and overexpressing the miR-182-5p endogenous levels and/or by the impact of the miR-182-5p manipulation in downstream regulation of cofactors, either co-activators or co-repressors of the AR signaling [41], that can affect the distinct tumor phenotypes. The gene discussed is AR; the disease is neoplasm.