A woman in her seventies presented with leukocytosis. Her white cell count was 33.87 × 10 3 /μL with 80.5% leukemia cells. Her bone marrow was replaced with peroxidase-negative leukemia blasts that were CD10 +/− , CD19 + , CD20 − , CD13 + , CD33 −/dim , CD34 + , CD117 −/dim , CD66c +/− , cytoplasmic (cy-) CD79a + , terminal doxynucleotidyl transferase + , and cy-IGHM − . G-banding revealed t(9;22)(q34;q11.2) as the sole chromosome abnormality, and reverse transcriptase polymerase chain reaction (PCR) and nucleotide sequencing confirmed that the fusion encompassed exon 19 of BCR and exon 2 of ABL1, which generate p230 micro (μ)-BCR-ABL1 mRNA. We treated her with a second-generation tyrosine kinase inhibitor, dasatinib, in combination with low-intensity chemotherapy (vincristine and dexamethasone) followed by consolidation, leading to a hematological complete response (CR) and 10 −4 level reduction of leukemia cell burden as measured by LightCycler ® -based real-time quantitative PCR assay. The patient received maintenance treatment with dasatinib followed by ponatinib and achieved hematological CR for 2 years and 8 months. This report showed that patients with the p230 μ-BCR-ABL1 fusion gene may present with not only chronic myeloid leukemia with mild clinical features but also Philadelphiapositive acute lymphoblastic leukemia (Ph+ ALL) with precursor B-cell immunophenotype; moreover, dasatinib-based induction, consolidation, and maintenance therapies are as effective for Ph+ ALL with μ-BCR-ABL1 as those with minor-and major-BCR-ABL1.