Interestingly, CLIP-seq data showed that ESRP1 (which was specifically upregulated in responders to ICB) can bind to 4 of the 34 atypical ASEs not undergoing NMD (i.e. in ASAP3, BUD23, SLC34A3, and SYTL1), which is significantly more than expected in case of random binding (odds ratio = 5.42; Fisher’s exact test, P = 0.0087), confirming that ESRP1 could indeed contribute to the generation of tumor antigens. The gene discussed is SLC34A3; the disease is neoplasm.