AR and neoplasm: Seminal studies have catalogued AR amplification, point mutations, and splice variant generation as drivers of therapeutic escape.[21, 22, 24] However, emerging evidence suggests that CAFs within the tumor microenvironment is a critical factor in treatment resistance.[25, 26, 27, 28, 29] Our findings identified STEAP4+ myoCAF as a therapeutically primed stromal subpopulation that emerges under enzalutamide (ENZ) selection pressure, demonstrating significant correlation with poor clinical outcomes.