The sequence that showed the greatest intersection with AmnSINE1 was SNHG14. Interestingly, SNHG14 is transcribed into a long noncoding RNA that hosts SNORD116, whose loss contributes to Prader-Willi syndrome (PWS) etiology (Ariyanfar and Good, 2022); indeed, many individuals affected by PWS also have cooccurring ASD (Dykens et al., 2011). The gene discussed is SNHG14; the disease is Prader-Willi syndrome.