different isoforms as increased predicted abundance of three splice variants were associated with AN, whilst the converse was true for the remaining four. None of these isoforms correspond to the canonical transcript; chr3:48 918 821:48 967 151 (Howe et al., 2020). In general, the ARIH2 gene is postulated to regulate ubiquitination (Kelsall et al., 2013; Marteijn et al., 2005) and post-transcriptionally modifies NLRP3 to reduce inflammatory activity (Kawashima et al., 2017), however, the functional specificity of particular splicing isoforms is less well characterised. This gene was also not significant in the TWAS, despite having a well-powered model of imputed expression in the PsychENCODE cortical samples. The only remaining transcripts surviving Bonferroni correction not proximally located to the chromosome 3 region were two isoforms of GPR75-ASB3 Readthrough (GPR75-ASB3). Decreased predicted abundance of these two isoforms was associated with AN.
