Analysis of Project Achilles datasets by Kryukov, et al.[48] alongside independent pooled shRNA screens of 390 cancer cell lines by Mavrakis, et al.,[47] revealed that MTAP loss, and concomitant accumulation of substrate S‐methyl‐5′‐thioadenosine (MTA), is responsible for inducing sensitivity to PRMT5 inhibition. The gene discussed is PRMT5; the disease is cancer.