DCAF8 (DDB1 and CUL4 associated factor 8) functions as a substrate receptor for CRL4 (Cullin-4 RING) E3 ubiquitin ligase complexes, facilitating the proteasomal degradation of target proteins 12. The protein plays critical roles in multiple cellular processes including muscle homeostasis, hematopoietic stem cell function, and cancer progression. In muscle tissue, DCAF8 promotes atrophy by targeting myosin heavy chain proteins for degradation through the CRL4A complex 1. In hematopoietic stem cells, DCAF8 prevents cellular senescence by mediating degradation of DOCK11, thereby regulating CDC42 activity and maintaining cell polarity; loss of DCAF8 leads to impaired stem cell function and accelerated aging 3. DCAF8 also regulates chr1 remodeling through LSH protein degradation, controlling ferroptosis and oxidative stress responses 4. In cancer contexts, DCAF8 demonstrates dual roles: it promotes DNMT3A degradation in hematologic malignancies 5 and contributes to cisplatin resistance in lung cancer through ERβ regulation 6. Additionally, DCAF8 targets myeloid leukemia factors MLF1 and MLF2 for degradation 2. The protein's expression levels correlate with disease progression across multiple cancer types, highlighting its potential as both a prognostic marker and therapeutic target.