RBM8A and myeloid neoplasm: Germline and somatic mutations associated with marrow hypocellularity are known to increase the risk of myeloid malignancies.14 In TAR, biallelic pathogenic variants in RBM8A are suggested to impair megakaryocyte differentiation.15 Increasing evidence also supports how genetic defects in spliceosome and RNA binding proteins drive the progression of myeloid malignancies.16 Loss of function of RBM8A may provide the correct conditions within the hematopoietic stem cell populations to drive myeloid malignancies.