Interestingly, in our stable MTHFD2 gene knockout lung cancer cell line using a CRISPR/Cas9 gene-editing technology, we did not observe proliferative difference between MTHFD2 deficient cells compared with wide type cells, but reduced gene expression was similarly as transient MTHFD2 knockdown, suggesting that cells may adapt to the low expression levels of MTHFD2 via using other alternate pathways rather than the mitochondrial pathway to compensate the growth and survive of cancer cells. This evidence concerns the gene MTHFD2 and lung carcinoma.