As described for the SNORD115 for modulation of 5-HT2c receptor editing,31SNORD116 deletion could impact IGFBP7 editing with consequences on its cleavage by proteases.18–21 Notably, PC1, product of PCSK1, could theoretically cleave at a furin site (R/K cleavage site at positions 94/95, Fig. S3).32 Thus, we first analyzed the presence of uncleaved and cleaved forms of IGFBP7 in the secretion medium of fibroblasts of PWS patients and controls. Here, IGFBP7 is linked to Prader-Willi syndrome.