Acute lymphocytic leukemia (ALL) is the most common cancer diagnosed in children and adolescents. Despite improved patient survival over the past fifty years, up to 20% of patients do not respond to therapy or develop resistance to treatment. Therefore, it is critical to identify new therapeutic targets to improve patient outcome. Approximately 4% of patients who present with ALL harbor a translocation between chromosomes 1 and 19 (t(1;19) pre-B-ALL). This translocation generates the TCF3-PBX1 fusion gene product, which arrests normal B cells in an immature developmental stage and maintains constitutively active kinase signaling. Small molecule tyrosine kinase inhibitors, like dasatinib, suppress these signaling pathways, but some leukemic cells can survive by activating rescue mechanisms. In response to dasatinib, the t(1;19) pre-B-ALL subtype exhibits upregulated ROR1 expression as an alternate mechanism to bypass kinase inhibition. ROR1 is required for t(1;19) pre-B-ALL survival, yet it cannot be easily targeted because ROR1 lacks kinase activity. Therefore, I sought to identify mechanisms important for ROR1 expression or signaling to determine additional proteins that may act as surrogate drug targets to inhibit ROR1.