Over 20 years ago, the discovery of Xist as a critical component of X chromosome inactivation revealed a fundamental role for long noncoding RNAs (lncRNAs) in epigenetic regulation during mammalian development and foreshadowed a fascinating connection between RNA and chromatin modification [1–3]. In the last decade, the field has exploded, heralded in part by a 2007 landmark paper from the group of Howard Chang [4] describing that knockdown of a lncRNA (Hox Antisense Intergenic RNA [HOTAIR]) was associated with loss of transcriptional repression from a locus on another chromosome in trans. HOTAIR lncRNA—encoded within the HOXC locus, although its expression seemed to be required for normal epigenetic silencing of HOXD genes—became one of the most well-known examples of functional lncRNAs in the field of developmental epigenetics. Interest intensified when a subsequent paper from the Chang lab [5] reported that targeted deletion of the orthologous locus in the mouse (Hotair) caused homeotic transformations underpinned by derepression of HoxD gene transcription in vivo. Discovery of new lncRNAs and exploration of their potential actions and effects during development and disease is a continued source of excitement [6,7]. But questions about the effects and actions of Hotair have been controversial, raised in part by work from the group of Denis Duboule [8]. This debate is addressed directly in the current issue of PLOS Genetics in a manuscript from Duboule’s laboratory [9] that reanalyzes Hotair mutant mice generated by the Chang lab, a formal comment in response to that manuscript from the Chang lab [10], and this perspective.