Meanwhile, five or fewer patients possess putative pathogenic variants in additional genes that have been implicated in myeloid malignancies, such as DNMT3A (a DNA methyltransferase) [23], KRAS (a GTPase) [24], CEBPA (a transcription factor involved in cell cycle regulation) [25], ASXL1 (a polycomb group protein involved in transcriptional regulation) [26], and SF3B1 (a splicing factor involved in U2 snRNP formation) [27] (Figure 2). This evidence concerns the gene CEBPA and myeloid neoplasm.