Recent sequencing data have shown that healthy human organs, such as skin, or blood can accumulate somatic mutations at a rate similar to that seen in many cancers [31,32,33,34,35,36,37], including known cancer-causing driver mutations such as canonical hotspot mutations in HRAS, KRAS, and NRAS, and/or inactivating mutations in TP53, FAT1, and NOTCH, but maintain physiological function of the epidermis [36,38]. This evidence concerns the gene FAT1 and cancer.