We then asked if STAT3 de-phosphorylation by 5-AZA could correlate with the upregulation of SOCS3 and/or PTPN6, as the former is a JAK/STAT inhibitor [26] and the latter is a tyrosine phosphatase [27] whose promoter methylation has been shown to contribute to STAT3 activation in other cancers. Here, SOAT1 is linked to cancer.