For example, amino acid substitution R882H in DNMT3A, often seen in patients having acute myeloid leukemia, appears to disturb DNMT3A function not only owing to a loss of enzymatic activity but also owing to the emergence of affinity between the active and inactive form of the protein, resulting in the formation of a catalytically inactive protein–protein conjugate [41,42,43,44,108]. Here, DNMT3A is linked to acute myeloid leukemia.