Many groups have reported the influence of pathological genetic variations of BRAF, such as c.1799 T > A and p.Val600Glu, on the progression of HPs, SSLs, TSAs, and KRAS pathogenic variants for HPs and TSAs, but these analyses were performed among patients with heterogeneous germline backgrounds [10–13]. The gene discussed is BRAF; the disease is Hermansky-Pudlak syndrome.