Importantly, this resistance may be therapeutically inhibited; for example, Casazza et al. demonstrated that a mutated, uncleavable version of SEMA3E (Uncl-Sema3E) bound to PlexinD1 reduced angiogenesis, growth and metastasis in mouse models transplanted with 4T1 cells and in tumours formed by the Lewis lung carcinoma cells (LLc), which are refractory to anti-VEGF treatments [60]. This evidence concerns the gene SEMA3E and lung carcinoma.