Indeed, a recent study found that ligand activation of AR profoundly decreases tumor burden in cell lines and mouse models of patient-derived luminal breast cancer, including those of endocrine and palbociclib (CDK4/6 inhibitor) resistant disease [121]. Ponnusamy et al. demonstrated similar findings using AR agonists or enobosarm, a selective androgen receptor modulator (SARM), in PDXs and tissue explants expressing either wild-type or mutant ER [131]. This evidence concerns the gene CDK4 and neoplasm.