Interestingly the two loss-of-function germlinealterations, c.816dup (p.(Ala273Serfs*9)) and c.952G>T (p.Glu318Ter) (Figure 2B), predicting early protein truncation/mRNAdegradation, are not associated with a POIKTMP phenotype, raising the possibility thatPOIKTMP, POH, and non-syndromic cancer predisposition are allelic disorders driven bydifferent types of FAM111B mutation. The gene discussed is FAM111B; the disease is cancer.