These variants have the ability to activate RNase L even without stimulation from double-stranded RNA, leading to RNA cleavage, changes in the transcriptome, and inhibition of translation.[17] Research by Thomas M[18] highlighted that the mRNA expression levels of OAS1, OAS2, and OASL among patients with SLE were significantly elevated compared to those in the normal control group, suggesting a role for OAS isoenzymes in the autoimmune mechanisms related to SLE. Here, OAS1 is linked to systemic lupus erythematosus.