BTK and B-cell chronic lymphocytic leukemia: This agent hijacks the CRBN-dependent ubiquitin-proteasome system to induce BTK degradation—a pivotal regulator of B-cell activity whose inhibition ameliorates B-cell malignancies (e.g., chronic lymphocytic leukemia [CLL]) and autoimmune disorders (e.g., graft-versus-host disease) (Figure 4).