SNORD116: SNORD116 is a long non-coding RNA (lncRNA) that plays a role in various biological processes. Deletion of SNORD116 in a mouse model lacking the lncRNA 116HG resulted in increased energy expenditure and dysregulation of circadian genes [PMC7215637]. SNORD116, along with SNORD115 and other snoRNAs, has been implicated in the pathogenesis of Prader-Willi syndrome (PWS) and schizophrenia [PMC6937981]. SETDB1 has been suggested as a potential therapeutic target for PWS treatment by disrupting its function selectively at the SNORD116 locus [PMC7176658]. The expression of Nhlh2 transcript levels was higher in mice lacking SNORD116 expression compared to wild-type mice [PMC9369261]. Deletion encompassing the snoRNAs within the SNORD116 cluster is sufficient to cause PWS [PMC4030979]. The 14q32.2 imprinted locus, which encodes snoRNAs similar to SNORD116, exhibits allele-specific chromatin decondensation in neurons [PMC7917289]. The role of SNORD116 in human energy homeostasis and growth requires further research [PMC7073628]. Transcriptional activation of the SNORD116 gene cluster is not controlled by the PWS-IC center and is not maternally silenced [PMC4742849]. RBFOX2 directly binds to SNORD116 snoRNA, suggesting its involvement in alternative splicing regulation [PMC8573313]. Multiple copies of SNORD116 are distributed within Ipw-A exons in mice [PMC8037846]. Dysregulation of snoRNAs, including SNORD116, has been observed in osteoarthritis and joint aging, suggesting their potential as biomarkers for these conditions [PMC9818347]. In conclusion, deletion or dysregulation of SNORD116 is associated with various physiological and pathological conditions, including energy expenditure, circadian rhythm, PWS, schizophrenia, and osteoarthritis [PMC7215637][PMC6937981][PMC7176658][PMC9369261][PMC4030979][PMC7917289][PMC7073628][PMC4742849][PMC8573313][PMC8037846][PMC9818347].