For example, the miRNA-mediated transcriptional repression of PRR11 and CAMK1D oncogenic drivers in melanoma biopsies (Figure S1) could be mechanistically compensated by the production of HGF aberrant transcripts (Figure S2), whose products may provide malignant cells with strong survival and growth advantages, and also confer resistance to selected therapeutic agents, such as Vemurafenib or its structural analog(s) [67,68,69]. The gene discussed is HGF; the disease is melanoma.