However, in our tumors, we cannot exclude the presence of secondary mutations, e.g., in BRAF or MEK1 per se or in other cancer-associated proteins, such as PIK3CA, CKIT, ALK and EGFR (as reported for BRAFi-associated cSCCs [9], or the presence of UV-induced signature mutations in genes such as RAC1, p53 and PTEN. This evidence concerns the gene TP53 and cancer.