We specifically chose the B-precursor acute lymphoblastic leukemia (B-ALL) as a study model since this disease is the most common childhood malignancy and the leading cause of cancer-related death in children and young adults. The most frequent B-ALL (∼22%) is characterized by the chromosomal translocation t(12;21)(p13;q22) that results in the fusion of two transcription factors, ETV6 and RUNX1, producing a functional fusion protein ETV6-RUNX1 previously known as TEL-AML1 [8, 9]. Specifically, we adapted permeabilization buffers and incubation time to investigate the presence of ETV6-RUNX1 fusion protein in pre-B cells, as well as ETV6-RUNX1 interaction with well-known cofactors.