The relatively new anti-cancer drug, crizotinib (Xalkori®, Pfizer), has created excitement in the research community. This drug has exhibited dramatic clinical benefits for select non-small cell lung cancer patients showing evidence of a mutation in the EML4-ALK gene. This gene mutation is present in 4 to 5 percent of non-small cell lung cancer patients. Crizotinib acts through a tyrosine kinase inhibition pathway, targeting the ALK and MET tyrosine kinases, to inhibit phosphorylation of activated ALK, which halts the ALK gene mutation and impedes metastasis. In phase I clinical trials, a 57 percent overall response rate was shown, and researchers calculated that the six-month progression-free survival was 72 percent.1 Therefore, patients treated with crizotinib had an increased survival rate when compared to conventional chemotherapy. Although the success rate of crizotinib is high, the mutated ALK gene has been shown to develop resistance to it. However, the predicted impact of this drug is still promising.