Recently, it has become evident that molecular targeted therapies may impact multiple functional interactions between tumour and immune response.27 As an example, the treatment with oral inhibitors of the mutated oncogene BRAF, in patients with metastatic melanoma, enhances lymphocyte activation, tumour infiltration and PD-L1 expression,28 supporting the exploration of associative clinical trials with checkpoint inhibitors. Here, BRAF is linked to neoplasm.