Several other studies have highlighted “extra-ribosomal” regulatory functions of RP involving their ability to bind to RNA targets and modulate processes, including pre-mRNA splicing and translation.12,14,15 These findings highlight a need to systematically investigate the contribution of RP inactivation, or reductions in their expression, to the etiology of myeloid neoplasms to gain insight into how the lost regulatory functions of RP might contribute to malignant hematopoiesis. The gene discussed is BLOC1S3; the disease is myeloid neoplasm.