Because PRMT5 is required to maintain proper splicing of full-length EP400 in a MYC-driven lymphomagenesis mouse model and has also been reported to promote full-length KAT5 splicing in hematopoietic cells (Koh et al, 2015; Hamard et al, 2018), we tested the effect of PRMT5 inhibition on their splicing in MCC cells using Western blot analysis. This evidence concerns the gene KAT5 and Merkel cell skin cancer.