We also found that putative tumor suppressors, such as FOXP1, STK4, and ATM, were frequently hypermethylated and silenced whereas oncogenes, such as UHRF1, MPZL1, CDK14, RACGAP1, and RAB13, were hypomethylated and overexpressed, suggesting that DNA methylation changes contribute to PTCL development. The gene discussed is ATM; the disease is neoplasm.