Cancer cells have been reported to utilize the JAK-STAT signaling pathway to increase PD-L1 mRNA expression, whereas RAC3 overexpression can activate JAK/STAT signaling through the PYCR1 axis to regulate PD-L1 expression, and thus suppress tumor immunity to provide favorable conditions for BCa progression (21, 31). The gene discussed is SOAT1; the disease is neoplasm.