AR and neoplasm: A genome-scale CRISPRi screen and orthogonal in vivo models identified the androgen receptor (AR) as a direct repressor of the MHC-I pathway; AR blockade transiently increased MHC-I expression, augmented T-cell–mediated tumor control, and suggested a therapeutic window in which AR inhibition could be paired with checkpoint blockade to convert low-visibility lesions into immunologically legible targets (153).