Furthermore, LOH of the APC has been firmly established as a mechanism for CRC tumorigenesis in patients with FAP, and a similar loss of the sole wild-type FLCN gene in this case appears to contribute to our patient’s development of cancer by similar rationale.24,25 Taken together, we postulate that our patient’s FLCN mutation and resulting folliculin protein dysfunction favored unchecked cell proliferation through its role in regulating AMPK and downstream targets, and this was possibly potentiated by dual mutations in APC. The gene discussed is APC; the disease is colorectal carcinoma.