Lnc‐fr91.3 was believed to be related to muscle rigidity in PD.11 In 2015, Carrieri et al demonstrated that antisense transcription regulated sense genes functioned at distinct regulatory levels in PD and could be used as a new therapeutic strategy.12 In 2016, Kraus et al analyzed the lncRNA expression profile of brain tissues from PD patients and normal subjects and found that significant differences in the expression of lncRNA‐p21, MALAT1, SNHG1, NEAT1, and H19. The gene discussed is NEAT1; the disease is Parkinson disease.