Overexpression of DCLK1-AL induces the expression of aldehyde dehydrogenase, stimulates CSC self-renewal, and enhances resistance to FDA-approved receptor tyrosine kinase inhibitors (sunitinib/sorafenib) and mammalian target of rapamyoin inhibitors (everolimus/temsirolimus) in renal cell carcinoma (RCC), suggesting its value as a target in this cancer. The gene discussed is DCLK1; the disease is renal cell carcinoma.