These findings, together with the discovered molecular mechanism of CDK11 inhibition,7 show that the different protein domains of the SF3B1 can be targeted with different effects on spliceosome assembly, but essentially the same on pre‐mRNA splicing and cellular proliferation and are consistent with a significant anti‐tumour potential of splicing inhibitors (now also including OTS964) and those targeting SF3B1/U2 snRNP specifically. Here, CDK19 is linked to neoplasm.