This process is mediated by the transcriptional activation effects of type I interferons, as PDL1 (CD274) is well‐documented as a type I IFN‐inducible gene.[23] We also recognize that the general ineffectiveness of PDL1 antibodies in treating colorectal cancer patients stems from the low expression levels of PDL1, which lack the necessary therapeutic target characteristics.[24] We hypothesize that the robust type I IFN response induced by ML323 following radiotherapy could enhance PDL1 expression. This evidence concerns the gene CD274 and colorectal cancer.