Studies have shown that in regulatory T cells (Tregs), IFITM3 can inhibit the transcription and phosphorylation of STAT1, while STAT1 can promote the transcription and expression of IFITM3[33] In hepatocellular carcinoma, both IFITM3 and STAT1 are highly expressed, and there is an interaction at the protein level between the two.[34] These findings suggest a potential reciprocal regulation between IFITM3 and STAT1 in different cellular contexts. This evidence concerns the gene STAT1 and hepatocellular carcinoma.