A functional genomics study mapped broad, convergent asciminib resistance mechanisms in BCR::ABL1 chronic myeloid leukemia. Researchers identified 279 resistance mutations, including changes outside the drug-binding pocket, indicating resistance can emerge through regulatory and structural pathways not previously emphasized. In parallel, a proteomics-focused study described how lipid remodeling in serum and colorectal tumor margins tracks disease progression, with the research emphasizing that systemic lipid chemistry and tumor-local lipid profiles shift differently as the cancer advances. Both reports point to how resistance biology and disease progression biomarkers are increasingly tied to complex network changes—supporting more targeted patient stratification and next-generation mechanism-based therapy design.