A previous report showed that IL-6/STAT3 inflammatory signaling axis induces the deacetylation of FOSL1 at the Lys-116 residue located within its DNA binding domain, leading to the increase of FOSL1 transcriptional activity and acquisition of colorectal cancer (CRC) stem-like properties (stemness) [17]. This evidence concerns the gene STAT3 and colorectal cancer.