To further explain the mechanisms of AZA resistance in PD patients, we observed possible impact of transcriptional dysregulation of other genes already implicated in cancer chemoresistance to deoxycytidine analogues, particularly significant upregulation of SLC29A1 [32] and downregulation of NT5C3B [84] in the PD vs. RD gene set comparisons (Figure S15). Here, NT5C3B is linked to cancer.