CD274 and Ataxia-telangiectasia: A possible mechanism in this study was attributed to the activation of the JAK/STAT3 pathway in an ataxia telangiectasia mutated-dependent manner,388 largely in agreement with the previous reports.368,389 Collectively, these observations provide strong evidence that the tight interactions between EMT programming and PD-L1 expression contribute critically to the development of resistance to either chemotherapeutics or targeted drugs, with or without the involvement of EMT/PD-L1-related immune escape.