We postulate that the transitional B cells which are expanded in APDS patients may not just be precursors to more mature B cells, but also include cells that are functionally equivalent to the CD19+B220− cells that we have identified in p110δE1020K mice and thus may also contribute to the increased susceptibility to S. pneumoniae infection and hence to the high incidence of bronchiectasis characteristic of this disease14. The gene discussed is CD19; the disease is activated PI3K-delta syndrome.