We propose that a gradual loss of MITF as sometimes observed during melanoma progression might be supplanted by a variable decrease in MYC turnover rather than transcriptional upregulation allowing for accumulation of MYC protein, which preserves CDK7 and acts as a compensatory switch mechanism to maintain transcriptional homeostasis and to modulate proliferative activity at the expense of melanocyte-specific gene activation (Fig. 6a–e and Supplementary Figure 8a). Here, MYC is linked to melanoma.