In this work, we developed an 18F-labeled lactate analogue and used it alongside L-[1-13C]lactate, D-[13C6]glucose and [18F]FDG to investigate the altered nutrient flux of tumors in the presence of the MCT1 inhibitor AZD3965: we present evidence that lactate is consumed by the DLBCL tumor model used, and, perhaps consequentially, AZD3965-mediated inhibition of lactate influx is reversed within 4 h of treatment. This evidence concerns the gene SLC16A1 and neoplasm.