According to the original EGIL scoring system BAL is defined when scores  are over two points for both myeloid and T- or B- lymphoid lineages. In 2008, WHO established a new and strict criteria standard for diagnosis of BAL. The presence of specific T-lymphoid antigens, cytoplasmic CD3 (cCD3), MPO and CD 19 became the most important standard for recognizing the lineage. Other B-lineage markers (CD22, CD79a, CD 10) and monocytic markers are also needed. Table 2 shows the method. Compared with the EGIL scoring system, the current  2008 WHO criteria applied less but more specific markers to define the lineage of the blasts,  and incorporated the intensity of markers expression into the diagnostic algorithm. The diagnosis of BAL is so difficult that sometimes is misdiagnosed with AML or ALL because the morphology thus the therapy would not have a good effect. Treatment
BAL is difficult to treat, most patients receive treatment based on the morphology of blasts and get AML or ALL induction chemotherapy. The induction drug for AML such as cytarabine and anthracycline, drug for ALL such as prednisolone, dexamethasone, vincristine, asparaginase or daunorubicin is common for BAL remission induction therapy. Recently, researches showed that using both myeloid and lymphoid induction therapy may be better for prognosis.Chemotherapy has strong side effects such as typhlitis, gastrointestinal distress, anemia, fatigue, hair loss, nausea and vomiting, etc. Thus, the different dose and times of chemotherapy for different individuals is important. If the patients enter fully remission, the consolidation with stem cell transplantation is highly recommended.
Pericardial or pleural effusion

Causes
The cause that directly leads to BAL is unclear. Exposure to radiation, chemical exposure, virus and genetics are the primary reasons proposed by researchers. Mechanisms
The mechanism of BAL is related to several mutations. The most common abnormalities are t(9;22) and MLL gene rearrangement at 11q23. T(9;22) affect the ABL gene at 9q34 and BCR at 22q11. The hybrid gene product ABL/BCR is an oncogene which could lead several types of leukemia including BAL. ABL/BCR could active several molecular pathways:

RAS signaling could be activated by BCR/ABL by GRB2 adaptor which interact with Y177 of BCR. Through AKT/PKB, PI3-K pathway could also be activated. STAT5, 1, and 6 has been reported that is a major molecular signaling event activated by BCR/ABL. Some focal adhesion complex (PAXILLIN, FAK0 could be activated by BCR/ABL with adaptor molecule CRK-L.
BCR/ABL could inactivate negative regulatory molecules PTP1B and Abi-1. Their inactivation is related with progression into blast crisis. BCR/ABL pathway could also active PI64K/Akt/STAT5 pathway which has anti-apoptotic activity. BCR/ABL induce cell adhesive and migratory abnormalities because the mutation will lead an abnormal response to chemokine SDF-1
MLL gene encode Histone-lysine N-methyltransferase (HRX), which is a histone methyltransferase. It is a positive regulator for gene transcription. It has been shown that associates with Host cell factor C1, CREB binding protein, WDR5, CTBP, MEN1, etc. The rearrangement of MLL are related with different kinds of aggressive acute leukemias. Most of biphenotypic leukemia in children is due to the rearrangement of MLL

Besides them, other gene abnormalities has been reported.