Although our data could not explicitly conclude that the sensitivities of MCL cells to PRMT5 inhibition are exclusively dependent on the particular genetic status, the PRMT5 inhibitors exerted more potent cytotoxicity in ATM, TP53, and/or CDKN2A-deficient CDX or PDX models, indicating that they are more dependent on PRMT5 which could be exploited as a potential therapeutic target for R/R MCL with heavy mutation burdens. This evidence concerns the gene ATM and mantle cell lymphoma.