However, in light of these findings, an alternative hypothesis must also be considered: that overexpression of N-terminally unmodified ICER under the regulation of the mitf promoter, may exert tumor-promoting effects in this context, and that the S35-41A mutation, by altering phosphorylation-dependent regulation, rescues the phenotype toward a less pathogenic or more neutral state. Here, MITF is linked to neoplasm.