In detail, the activation of JAK1/STAT3 was initiated by enhanced p300 (histone acetyltransferase)‐mediated STAT3 acetylation, which, in turn, promoted the phosphorylation of JAK1 through DNMT3b hypermethylation‐dependent Src homology region 2 domain‐containing phosphatase‐1 (SHP‐1) silencing, whereas the sustained activation of JAK1/STAT3 signaling was maintained by DNMT1.[85] Beside, the relationship between abnormal metabolism and epigenomic alterations of CAFs has emerged as a threat to cancer progression. The gene discussed is STAT3; the disease is cancer.