Introducing this mutant into PRMT5-inhibited or PRMT5-deficient MCC cells would clarify whether the loss of PRMT5-dependent methylation disrupts the binding of SRSF1 to the m6A reader YTHDC1 and consequently fails to restore KAT5 exon 5 inclusion or other PRMT5-sensitive splicing events. Here, KAT5 is linked to Merkel cell skin cancer.