EGR1 and acute myeloid leukemia: Mechanisms underlying the potentiating effects of the above compounds on 1,25D-induced differentiation of AML cells have been extensively studied and shown to involve the activation of various signaling kinases, such as protein kinase C [15, 28, 29], phosphatidylinositol 3-kinase [28]; MAPKs, including ERK [7, 15, 28, 29] and JNK [20], as well as the transcription factors AP-1 [7, 11, 20], Egr-1 [8, 20], and Nrf2 [11].