Huang et al. demonstrated that abnormal activation of the IL-6 (interleukin-6)/STAT3 (signal transducer and activator of transcription 3) signaling pathway promotes transcriptional repression of SOCS3 by increasing DNMT1 activity, which can lead to the growth and metastasis of pancreatic cancer. This evidence concerns the gene STAT3 and pancreatic neoplasm.