The results showed that SHMT1-mediated cytosolic 1C metabolic flux is the primary source of 1C units in a series of cancers, including T cell acute lymphoblastic leukemia, glioblastoma, and non-small-cell lung carcinoma under normal physiological folate concentration, whereas mitochondrial 1C flux is overly repressed, suggesting that tumor-specific reliance on cytosolic 1C flux depends on poor folate availability. This evidence concerns the gene SHMT1 and non-small cell lung carcinoma.