The mutational status of platelet-receptor PEAR1 was recently identified as a major factor for survival of young patients with Acute Myeloid Leukemia. While studies show that wildtype PEAR1 regulates hematopoiesis, little is known on how PEAR1’s mutational status may impact downstream pathway proteins’ activity. We generated triplicate Ba/F3 cell lines using retroviral vector transduction, stably expressing empty vector, wildtype, or mutated PEAR1. Further experiments will help validate the changes in identified pathway proteins across lines using Western blots. Subsequent drug treatments will evaluate the impact of PEAR1’s mutational status on cell survival.