HIF1A and colorectal cancer: Interestingly, Chiacchiera et al.14 found that inhibition of p38α initiated a switch from HIF1α- to FOXO-dependent transcription in colorectal cancer cells.14 In our study, although protein levels of HIF1α were higher in peroxide-treated cells compared with untreated controls regardless of extracellular glucose, HIF1α was only transcriptionally active in cells cultured in low glucose.