The functional synthetic lethality interaction between MTAP deficiency and PRMT5 and its potential in the treatment of cancer has been recently reviewed.[5] Both landmark studies by Mavrakis, et al.[47] and Kryukov, et al.[48] effectively demonstrated that in a broad range of MTAP‐deficient cancer cells, levels of PRMT5 inhibitory cofactor molecule MTA were already significantly elevated, directly affecting endogenous PRMT5 activity. Here, PRMT5 is linked to cancer.