This STEM project represents a pivotal endeavor in cancer research, aimed at unraveling the complex puzzle of drug resistance in chronic myeloid leukemia (CML). CML poses a formidable challenge due to the gradual loss of treatment effectiveness over time, necessitating a deeper understanding of the underlying molecular mechanisms driving resistance. By honing in on mutations within the BCR-ABL kinase domain, the primary driver of uncontrolled white blood cell proliferation in CML, this study embarked on a meticulous exploration into the structural alterations induced by these mutations. Through a multifaceted approach encompassing structural biology tools such as PyMOL, computational modeling, and statistical analysis including a one-way ANOVA test, the investigation delved deep into the intricate interplay between molecular alterations and therapeutic outcomes. The identification of specific mutations, notably T315I, as significant contributors to TKI resistance underscored the urgency of targeted therapeutic strategies to overcome this challenge. This research not only sheds light on the molecular basis of drug resistance but also opens new avenues for the development of tailored treatments that can outmaneuver cancer's adaptive defenses. Ultimately, this project holds promise for enhancing treatment efficacy and improving outcomes for individuals grappling with CML, offering renewed hope in the relentless fight against leukemia.