The most promising candidate genes were POLE, ERCC6, RAD54L, and PALB2. The POLE variant (c.1847G > A; p.Arg616His) identified in LLS20 was outside the exonuclease domain, and its respective tumor was not hypermutated and did not present any mutational signatures previously associated with POLE variants. The gene discussed is POLE; the disease is neoplasm.