Finally, we demonstrated that xenograft tumor growth suppression by the HIF2α antagonist PT2399 is reduced by expression of a mutant BMAL1 that does not interact with HIF2α and is highly dependent on the time of day at which PT2399 is delivered, suggesting that BMAL1 expression and/or physiological circadian rhythms could contribute to differential sensitivity to HIF2α antagonist drugs in ccRCC. Here, EPAS1 is linked to neoplasm.