Indeed, Lin28a/b overexpressing in NIH/3T3 cells led to tumor formation in nude mice and was linked to depletion of mature let-7. As a consequence, oncogenic let-7 targets such as c-Myc and N-Ras were de-repressed, and, since c-Myc itself transcriptionally activates various oncogenic miRNAs as well as Lin28b, a positive feed-forward loop is established [12,60]. The gene discussed is LIN28A; the disease is neoplasm.