SOAT1 and neoplasm: Since promoter region hypermethylation is present in NKTCL, in vitro studies indicate that reversal of methylation by decitabine induces expression of key candidate genes involved in tumor suppressor (PRDM1), pro-apoptosis (BIM and SAPK), JAK-STAT pathway (SOCS6, ZFHX3, and PTPN6), and cell growth inhibition (CD300A) etc., leading to increased NK-cell death [27, 46].