Given the upregulation of Gal‐1 following BRAF inhibition in melanoma cell lines and T‐cell apoptosis‐inducing activity of this protein, we hypothesized that increased expression/secretion of Gal‐1 in BRAF inhibitor‐treated patients would facilitate deletion of tumor‐infiltrating T cells and might represent a mechanism of disease immune escape and progression. The gene discussed is BRAF; the disease is melanoma.