This correlation is supported by our findings that: (1) increased intracellular spermidine could inhibit CRC cell growth in a concentration-dependent manner; and (2) restoration of spermine or putrescine levels in SMS-deficient CRC cells did not alter spermidine accumulation or reverse cell growth inhibition by SMS deletion, but re-expression of SMS resulting in a marked decrease in the spermidine level did restore cell growth. This evidence concerns the gene SMS and colorectal carcinoma.