The interactions of the mTOR cascade with STAT-mediated signaling (e.g., in immunity [15]), and the roles attributed to STAT3 and STAT1 in promoting PD-L1 expression [16,17,18,19], have led us to inquire in depth about the potential involvement of STAT3 and STAT1 in PD-L1-mediated effects in breast cancer cells. The gene discussed is SOAT1; the disease is breast cancer.