The majority of patients with myeloid malignancies and RCs with NGS data (n = 58) possess at least one candidate pathogenic mutation in TP53 (n = 39 patients; 67.2%), which is normally involved in cell signaling in response to stress; TET2 (n = 8 patients; 13.8%), which is normally involved in catalyzing the conversion of methylcytosine to 5-hydroxymethylcytosine; and/or NRAS (n = 7 patients; 12.1%), which normally functions as a GTPase (Supplementary Table S1). This evidence concerns the gene NRAS and myeloid neoplasm.