For this combination, one may speculate that after an initial depletion of tumor cells by erlotinib outgrowth of drug resistant tumor cell clones, harboring resistance mutations such as T790M was prevented by simultaneous inhibition of tumor endothelial cell growth and their secretion of pro-tumorigenic factors, such as SDF-1, by bevacizumab [65, 122]. Here, CXCL12 is linked to neoplasm.