MAX and cancer: HIF1A and MYC interplaying is well-known in cancers [10]; under hypoxia, HIF1A represses MYC through different suggested ways, such as activating MXI-1, which is an antagonist of MYC with regards to mitochondrial biogenesis [50, 51], or by competing with MYC in binding directly to MAX, without which MYC does not carry out its function [48], or by binding to Sp1 to result in the displacement of MYC from Sp1 complexes and consequently decreased MYC activity [52].