Fam220a, a gene of yet-fully-characterized function, is putatively involved in multiple biological processes. It is thought to activate STAT family protein binding activity, participate in the negative regulation of transcription through RNA polymerase II, and protein dephosphorylation [2].

In the context of renal injury-associated atherosclerosis, it was identified as a putative target of miR-92a-3p. In apolipoprotein E-deficient (Apoe-/-) mice with renal damage (5/6 nephrectomy), dual inhibition of endothelial miR-92a-3p and miR-489-3p led to a significant increase in Fam220a expression in aortic endothelium. Gene reporter assays further validated Fam220a as a direct target of miR-92a-3p. In human coronary artery endothelial cells, over-expression and inhibition of miR-92a-3p decreased and increased FAM220A expression, respectively, with miR-92a-3p overexpression increasing STAT3 phosphorylation, likely through direct regulation of FAM220A [1]. Additionally, transcriptome sequencing in a study related to Parkinson's disease showed that Fam220a was differentially upregulated upon Dyrk1a knockdown, with differentially expressed genes enriched for neuroactive ligand-receptor interaction, vascular smooth muscle contraction, and melanogenesis-related pathways [2].

In summary, Fam220a seems to be involved in regulating STAT3-related signaling pathways, as seen in both atherosclerosis and potentially in Parkinson's disease-related mechanisms. Studies in mouse models have provided insights into its role in these disease-associated processes, highlighting its potential importance in understanding and treating such conditions.