The human genome sequencing effort has taught us that it takes relatively few genes to build a human being. Complexity arises from the combination of these building blocks into genetic programs that are finely tuned in space and time during cell and tissue differentiation. A major part of this regulation is performed by microRNAs (miRNAs), small RNA molecules encoded by the genome that are not translated into proteins; rather, they control the expression of genes. Deregulation of miRNA function has been implicated in human diseases including cancer and heart disease (1, 2). On page 1220 of this issue, Kim et al.(3) suggest that miRNAs are essential for maintaining dopaminergic neurons in the brain, and thus could play a role in the pathogenesis of Parkinson’s disease. Similar to classical genes, regions of the genome that encode miRNAs are transcribed in the cell nucleus. Nascent miRNA transcripts are initially processed into long (up to several kilobases in length) precursor miRNAs that are then sequentially cleaved by two enzymes, Drosha and Dicer, into small functional RNAs (∼ 22 nucleotides). These miRNAs are subsequently incorporated into an RNA-induced silencing complex (RISC), which suppresses the translation and/or promotes the degradation of target messenger RNAs (mRNAs)—RNA molecules that encode proteins—by binding to their 3'-untranslated regions (3'-UTRs)(4). miRNAs are abundant in the brain and are essential for efficient brain function. In this regard, expression of a brain-specific miRNA (miR-124a) in nonneuronal cells