Accurate detection of chromoanagenesis- or chromothripsis-induced single-nucleotide polymorphisms (SNPs) in antiapoptotic genes is crucial for understanding their impact on protein structure and function during cancer progression. To address this issue, we developed a computational model using the BCL2 gene to investigate the effects of chromothripsis-induced SNPs on the structure and function of antiapoptotic proteins. This chapter demonstrates the utility of our computational pipeline in predicting Bcl-2 structural stability and protein–protein interactions under high mutation rates associated with extensive genomic rearrangements. Additionally, we provide practical recommendations for effective structural analysis of mutated proteins. In addition to our in silico methodology, users can incorporate supplementary computational approaches, such as molecular dynamics simulations, for a more detailed analysis of the effects of mutations on protein structure.