These incidents might be attributed to enhancing Pi transport in A549 cells by elevating the expression of SLC34A2. From this it was hypothesized that the downregulation of SLC34A2, expressed primarily in AT II cells, might cause abnormal AT II cells to escape from complement-associated immunosurveillance and abnormally express certain tumor-suppressor genes, inducing development of these cells into lung adenocarcinoma. Here, SLC34A2 is linked to neoplasm.