Similar to other investigations that demonstrated roles for the mTOR pathway in mediating PD-L1 activities [83,84], we also noted the activation of mTOR in our system (data not shown); however, our experiments using general inhibitors of two large receptor families that contribute much to tumor progression—GPCRs that signal via Gαi and Ras-activating receptors—substantiated the roles of previously unidentified pathways in controlling the tumor-intrinsic activities of PD-L1 in breast tumor cells. This evidence concerns the gene CD274 and breast neoplasm.