For example, in pancreatitis, penetrance may vary from virtually 100 % in the case of the most common mutations in the cationic trypsinogen gene (PRSS1) gene, via an intermediate level for SPINK1 and CFTR mutations, to the much more subtle risk conferred by the disease modifiers, namely variants in the chymotrypsin C (CTRC), calcium-sensing receptor (CASR) and anionic trypsin (PRSS2) genes, which can only be identified through large cohort studies (Lerch et al. 2010). The gene discussed is PRSS1; the disease is pancreatitis.