In our case, each tumor tissue had somatic mutations reported in TCGA, from which we hypothesize that although the mutation in CHEK2 is the pathogenic mutation in the patients with LFS or LFS-L, finally either the tumor is more associated with the accumulation of somatic mutations in a particular organization or the mutation in CHEK2 induces chromosomal instability and somatic mutation accumulation. The gene discussed is CHEK2; the disease is neoplasm.