KDM5A knockdown reduced the number of drug-resistant cells and promoted the expression of P21 and BAK1, implying that KDM5A may induce cell resistance by regulating P21 and BAK1. In addition, the knockdown of KDM5A or treatment with KDM5 inhibitors, such as KDM5-C49 or KDM5-C70, augmented the sensitivity of endocrine-resistant luminal BC cells to fulvestrant [101]. The gene discussed is BAK1; the disease is breast cancer.