Taken collectively, niclosamide interferes with amino acid nutrition in cancer cells by at least three mechanisms: inhibition of macropinocytosis of extracellular proteins via intracellular acidification, direct inhibition of SLC38A5-mediated amino acid entry into cells and also inhibition of SLC38A5-dependent micropinocytosis, and interference with the driving force for SLC15A1-mediated cellular uptake of small peptides arising from degradation of extracellular proteins. This evidence concerns the gene SLC38A5 and cancer.