Among them are loss-of-function mutants in hai1a [20,21,22,23,24,25], in which epidermal pre-neoplasm but also concomitant tumor-suppressive processes occur as direct consequences of increased Matriptase-1 activity, mediated by the Protease-activated receptor 2b (Par2b) and a linear EGFR (Epidermal growth factor receptor)–PLD (Phospholipase D) signal transduction pathway [20]. This evidence concerns the gene GPLD1 and neoplasm.