We found that TRDMT1, NSUN5 and DNMT1 showed homozygous amplifications and TET2, NSUN2, DNMT3B and DNMT3A showed homozygous deletions in AML patients, while almost all m5C regulators showed heterozygous amplifications (except for NSUN5 and NOP2) and heterozygous deletions (except for NSUN4, YBX1, TET3, DNMT3A and ALKBH1) (Figure 4E). The gene discussed is ALKBH1; the disease is acute myeloid leukemia.