Mixed Phenotype Acute Leukemia (MPAL) is an understudied subtype of leukemia that shares features of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML). Unfortunately, patients with MPAL have been left out of clinical trials, leading to a lack of standardized treatment. Instead, they may receive chemotherapies normally used for ALL or AML, and their outcomes remain poor. A better understanding of the disease is essential to design more efficient and targeted therapies. Rearrangements of the ZNF384 gene are a common genetic change in childhood MPAL. These gene changes, which lead to the production of abnormal fusion proteins, are known to drive the development of childhood leukemia. While studies have shown that ZNF384 fusion proteins can turn normal bone marrow cells into leukemia cells, it remains unclear how exactly this occurs. I discovered that the fusion partner protein sequences were full of disordered regions. Most protein domains have a specific shape that helps them perform their function. Instead, disordered regions are flexible and unstructured, which makes it easy for them to interact with other molecules. In particular, they have been shown to interact with a protein complex called SWI/SNF, which is essential to regulate the 3D architecture of DNA and gene expression. I hypothesized that ZNF384 fusion proteins are dependent on SWI/SNF to cause leukemia and found that inhibition of SWI/SNF impaired the growth of MPAL cells in vitro.