Under hypoxic conditions, as mimicked in CAFs, elevated MCT1 expression due to loss of TP53 promotes lactate export, whereas under conditions of additional glucose deprivation - as may be simulated in cancer cells due to heightened energy demands - MCT1 expression promotes lactate import. Through this differentiated mechanism, cancer cells could profit greatly from the lactate efflux originating from adjacent CAFs. This evidence concerns the gene TP53 and cancer.