For example, colorectal patients harbored recurrent hypermethylation of extracellular matrix components of the TSGs CDM2, COL18A1 and MMP2,33 and lymphoma patients frequently exhibited elevated promoter methylation levels of CAST, NCOA4, LYN and DNMT3A. Interestingly, DNMT3A is frequently mutated in acute myeloid leukemia patients and so its epigenetic silencing in lymphoma patients could also drive tumorigenesis in this context.34 In addition, as LYN functions as a B-cell receptor regulator, its repression could directly participate in altered B-cell behavior and tumor formation.35 The gene discussed is COL18A1; the disease is acute myeloid leukemia.