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Despite the clinical success of ADCs\u2014with 4 FDA\u2010approved agents to date, and 15 for the entire cancer landscape\u2014their therapeutic durability is frequently undermined by acquired resistance. Rather than arising solely from tumor\u2010intrinsic alterations, ADC resistance reflects a multi\u2010layered process shaped by dynamic interactions among cancer cells and the tumor microenvironment (TME), with activation of adaptive signaling networks. For example, stromal architecture, vascular heterogeneity, and immune modulation intersect with clonal evolution, phenotypic plasticity, and pathway reprogramming, thereby constraining ADC delivery and activity. Cutting\u2010edge technologies such as spatial omics, single\u2010cell profiling, functional genomics, and patient\u2010derived models are redefining how these resistance mechanisms are mapped and understood in situ. 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