MYBL2 (MYB proto-oncogene like 2) functions as a transcription factor that regulates multiple cellular processes critical for cancer development and progression. MYBL2 controls cell survival, proliferation, and differentiation by modulating key signaling pathways 1. In cancer contexts, MYBL2 acts as an oncogenic driver through several mechanisms. It disrupts the Hippo-YAP pathway by regulating RhoA GTPases and LATS1 kinase activity, promoting castration resistance and metastatic potential in prostate cancer 1. MYBL2 also maintains cancer stem cell properties and facilitates differentiation programs, as demonstrated in bladder cancer where MYBL2-high cancer stem cells contribute to immune checkpoint blockade resistance through CCL15-mediated macrophage polarization 2. The protein regulates stemness-associated genes including TP63 and TEAD4, while promoting extravillous trophoblast differentiation through AJUBA expression 3. Clinically, MYBL2 overexpression correlates with poor prognosis across multiple cancer types. High MYBL2 levels associate with advanced tumor stage, metastatic relapse, and reduced survival in prostate and breast cancers 14. Additionally, MYBL2 dysregulation contributes to pregnancy complications, with decreased expression linked to recurrent spontaneous abortion through impaired trophoblast function 3. These findings establish MYBL2 as both a prognostic biomarker and potential therapeutic target.