As shown in the study by Beltran et al., the knockdown of endogenous GLUT3 expression is sufficient to completely abolish the effect of ascorbic acid.26 In addition, overexpression of GLUT1 is associated with chemoresistance and an inferior overall survival, which indirectly suggests that expression of GLUT1 is not beneficial compared with the expression of GLUT3.27 Taken together, GLUT1 was not able to compensate for and transport vitamin C to enhance TET activity in AML cells. Here, SLC2A3 is linked to acute myeloid leukemia.