However, irrespective of the underlying molecular action, it is anticipated that intervention in the poor prognosis, PRKCB-mutant form of ATLL should involve inhibition of catalytic activity; for the common D427N PKCβ mutant characterised here, this would require development of novel mutant-engaging drugs given the weak activity of current inhibitors. This evidence concerns the gene PRKCB and adult T-cell leukemia/lymphoma.