SPINK1 and neoplasm: These mechanisms include inhibition by pancreatic secretory trypsin inhibitor (PSTI), also known as a serine protease inhibitor Kazal-type 1 (SPINK1) or tumor-associated trypsin inhibitor (TATI) (Hirota et al., 2006), and degradation by chymotrypsin-C (CTRC) (Binker et al., 2015) and the lysosomal hydrolase cathepsin-L (Wartmann et al., 2010).