STAT1 and neoplasm: It suggests that irradiation could primarily drive STAT1 phosphorylation towards a pro‐apoptotic axis, promoting tumor shrinkage, potentially leading to the decoupling of IDO1 expression from STAT1‐dependency by either altering the signaling dynamics within the tumor microenvironment, leading to changes in the regulatory control of IDO1 expression or by alternate STAT1‐independent pathways, such as direct DNA damage response mechanisms or other transcription factors activated by radiation.