Consistent with this notion, a previous study detected increased levels of LINGO1 in the cerebellum ET patients.25 Thus, while the outcome of duplication of the other genes located within the genomic region defined in our study requires further exploration, our data, combined with existing studies of LINGO1 in ET, indicate that hypermorphic mutation leading to increased transcriptional or protein activity of LINGO1 represents a likely pathogenic cause. The gene discussed is LINGO1; the disease is essential thrombocythemia.