Given that O2 levels vary widely across sub-domains of solid tumors [owing, for example, to rapid cell division and aberrant tumor angiogenesis and blood flow (Bertout et al., 2008)], it will be interesting to explore whether JFK is a co-target of both HIF-1α and HIF-2α, perhaps under different severities of hypoxia, in different tumor sub-domains, or at different stages of breast cancer development. This evidence concerns the gene EPAS1 and breast carcinoma.