Fam220a, whose functions are still being explored, is predicted to activate STAT family protein binding activity, participate in the negative regulation of transcription through RNA polymerase II, and protein dephosphorylation [2]. It has been associated with the STAT3 immune response pathway, suggesting its potential importance in immune-related biological processes [1]. Animal models could be valuable for further functional studies of Fam220a.

In a study on renal injury-associated atherosclerosis, Fam220a was identified as a putative target of miR-92a-3p. In vivo miRNA inhibition led to a significant increase in Fam220a expression in aortic endothelium. In human coronary artery endothelial cells, over-expression and inhibition of miR-92a-3p respectively decreased and increased FAM220A expression. Moreover, miR-92a-3p overexpression increased STAT3 phosphorylation, likely through direct regulation of FAM220A, a negative regulator of STAT3 phosphorylation [1]. In another study related to Parkinson's disease, transcriptome sequencing showed that Fam220a had differentially upregulated expression when Dyrk1a was knocked down, and the differentially expressed genes were enriched for the neuroactive ligand-receptor interaction, vascular smooth muscle contraction, and melanogenesis-related pathways [2].

In conclusion, Fam220a seems to play a role in the regulation of the STAT3 pathway, as indicated by in vivo studies in atherosclerosis and Parkinson's disease-related models. Its function as a negative regulator of STAT3 phosphorylation and its association with multiple pathways suggest its importance in both immune-related and neurodegenerative disease processes. Research on Fam220a using these models contributes to understanding the underlying molecular mechanisms of such diseases.