In prostate cancers, the dual loss of TP53 and RB1 promotes lineage plasticity in vitro and facilitates transdifferentiation to SCNC in vivo [12, 13], while in urothelial cancers, TP53 and RB1 loss occurring after the initial tumorigenesis is essential for the transdifferentiation into bladder small‐cell carcinoma [14]. This evidence concerns the gene TP53 and prostate cancer.