RBPMS is an RNA-binding protein that functions primarily as a regulator of pre-mRNA alternative splicing (AS) 1. The protein recognizes tandem intronic CAC motifs in target genes and associates with spliceosome factors and other RNA-binding proteins like RBM20 to modulate AS events 2. In cardiac tissue, RBPMS is essential for maintaining normal cardiomyocyte function. Cardiac-specific loss of RBPMS causes severe contractile defects and dilated cardiomyopathy by dysregulating AS of sarcomeric genes including Ttn, Pdlim5, and Nexn 2. During development, RBPMS mediates cardiomyocyte binucleation through Pdlim5 isoform switching, and its loss causes premature binucleation and cell cycle arrest, leading to congenital cardiovascular defects 3. RBPMS also promotes contractile vascular smooth muscle cell differentiation through MYOCD alternative splicing, thereby inhibiting atherosclerotic plaque development and postintervention restenosis 4. Beyond cardiac function, RBPMS acts as a coactivator of SMAD transcriptional activity in TGFβ signaling 1. In bladder cancer, RBPMS downregulation correlates with poor prognosis, and restoration of RBPMS suppresses cancer cell migration by attenuating MYC pathway activity through ANKRD10 alternative splicing 5. In retinal ganglion cells, RBPMS localizes to soma under normal conditions but redistributes to dendrites and axons under hypoxic stress, suggesting roles in neuronal stress responses 6.