Around a century ago, Aldred Scott Warthin documented the first known family with what is now called Lynch syndrome (Warthin 1913). In 1925, he published further research on “cancer family G” (Warthin 1925). After Warthin’s death, in 1931, colleagues Hauser and Weller continued the work in 1936, but research interest waned until the 1960s. The concept of a hereditary colorectal cancer distinct from familial adenomatous polyposis remained uncertain until Henry T. Lynch detailed several families in 1966–1967, coining the term “Cancer Family Syndrome.” In 1973, C. Richard Boland expanded the documentation, introducing the terms Lynch syndrome I and II to distinguish colorectal-only cases from those with additional cancers. Lynch later proposed the term “hereditary non-polyposis colorectal cancer” in 1985, which persisted until genetic discoveries refined the definition of Lynch syndrome (Lynch et al. 1985a, b; Boland and Lynch 2013). Lynch syndrome (LS) is characterized by a higher risk of developing colorectal cancer as well as malignancies of the endometrium, ovaries, stomach, small intestine, urinary system, bile ducts, brain (glioblastoma), skin (sebaceous adenomatous, sebaceous carcinomas, and keratoacanthomas), pancreas, and prostate (Idos and Valle 1993). Lynch syndrome is the leading inherited cause of colorectal cancer (Bhattacharya et al. 2024). In the United State, the prevalence of LS is approximately 1:279 people, which equals roughly 1.2 million adult individuals (Hampel and Hall 2018).