The direct and significant association between BRAF mutations and a higher level of PD-L1 expression in thyroid cancer, as also described in other human cancers, such as NSCLC, is probably due to a relatively higher TMB level [21,22] or the induction of epithelial/mesenchymal (EM) transition with subsequent greater tumor immune evasion, as a consequence of AXL-PI3Kinase-PD-L1 signaling axis activation, a mechanism recently described in head and neck and lung cancer [23,24]. This evidence concerns the gene BRAF and non-small cell lung carcinoma.