Some BETi have not only entered clinical trials for hematologic malignancies such as AML, ALL, and CML but have also initiated clinical trials for various solid tumors, including breast cancer and colorectal cancer, demonstrating potential in inducing tumor cell apoptosis and tumor regression.[4] However, resistance to BETi targeting BRD4 is common in solid tumors.[5] Recent research has demonstrated that CAFs‐activated stromal signaling induces BRD4 phosphorylation in tumors, leading to increased chromatin binding and reduced binding to BETi, thus contributing to resistance. This evidence concerns the gene BRD4 and chronic myelogenous leukemia, BCR-ABL1 positive.