FAT1 and neoplasm: Interestingly, like TP53, the mode of FAT1 inactivation is quite unique, compared with most tumor suppressors; ~22% and 75% of FAT1 genomic alterations are missense and truncating/nonsense mutations, respectively, both of which facilitate the synthesis of a stable mutant FAT1 protein which accumulates in the plasma membrane and nucleus of the aggressive and/or cisplatin-resistant OSCC cells.