Hence, in view of the negative cross-regulation between MITF and the oncomir-221&222 [18, 21] and considering the direct targeting of SCD5 by miR-221&222 themselves, we might suggest a self-sustaining circuitry connecting these molecules that, in presence of SCD5, favors the MITF differentiative side, eventually moving the balance from tumor progression toward a less malignant phenotype (Figure 7). Here, SCD5 is linked to neoplasm.