Metabolic reprogramming provides sufficient energy and metabolic intermediates for tumorigenesis and has become a promising area in the development of anticancer drugs.[2] We discovered that the SHMT1/2 inhibitor SHIN1, which blocks serine catabolism, significantly hindered the proliferation of lung adenocarcinoma cells by using a screening compound library that directly inhibits metabolic enzymes. The gene discussed is SHMT1; the disease is lung adenocarcinoma.