In 2019, a 69-year-old man was referred due to incremental neutrophilic leukocytosis and fatigue since several months. Medical history included diabetes mellitus type 2. Medical therapy comprised sitagliptin/metformin (50 mg/1000 mg BID), rosuvastatin (10 mg QD), and allopurinol (100 mg QD). Biochemical analysis showed normocytic anemia with concurrent neutrophilic leukocytosis and 2.7% blasts. Electrophoresis and immunofixation indicated MGUS (IgG lambda type). Bone marrow biopsy showed hypercellularity with blast excess (20%). Cytogenetic analysis identified a complex karyotype with monosomy of chromosome 7, trisomy of chromosome 14, and deletion of p12 ( Table 2 ). CSF3R (44%), SETBP1 (45%), and U2AF1 (42%) appeared mutated. The diagnosis of AML secondary to CNL was made. Complete morphologic and cytogenetic remission was obtained after eight cycles of decitabine. Planned allogeneic HSCT was postponed due to flu and the SARS-CoV-2 pandemic. The patient relapsed several months later. Cytogenetic analysis detected the reoccurrence of previous described mutations in combination with a new translocation t(17;22) ( Table 2 ). Despite that no CR was obtained after remission-reinduction, allogeneic HSCT was performed. Bone marrow analysis 2 and 4 months afterwards showed no blast excess; mutated CSF3R was absent. The patient recovered and is currently, more than 2 years after HSCT, in CR. Paraproteinemia and neutrophilic leukocytosis did not reoccur.