By using R-banding karyotypic analysis technique, the bone marrow (BM) cells were performed in 223 hematopoietic malignacies and 105 diopathic throbocytopenic purpura (ITP), which served as control. The following results were obtained: (1) Nonrandom chromosome loss (NCL), such as, -11, -14, -21, etc, which were found in the affected members of leukemia families, were found in about 30% sporadic ANLL, MDS and about 50% ALL, espedislly in 100% (5/5) CLL, but not found in ITP (P < 0.001). These results indicated that the familial nonrandom chromosome loss were associated with leukomogenesis. (2) Because most of BM cells are hypodiploed and have the same kinds of NCL in each cases of CLL, which can develop into ALL, ANLL and also cancers, ALL BM hypo- and hyper-diploid and/or polyploid cells might be origin of hypodiploid cells. (3) 28% (6/21) of pediatric patients with AL, MDS, or FA (Fanconi Anemia) have one parent, who have up to 30% BM hypodiploid cells and similar kinds of NCL and also have the rearrangement of C-erbB and abnormal proliferation of BM. The NCL were found in the three consecutive generations of a family with 5 ALL among 10 members of third generation. It indicated that the familial NCL might be inherited and be coded by a unknown gene alteration, which might be related to leukomo and carcinogenesis, because there are genes or their candidates for leukemia in the chromosomes 11, 14 and 21. (4) Based on the works of my colleages and I, the model of leukomo and carcinogenesis was proposed and the relationship between chromosome monosomy, deletion, translocations and leukomogenesis were showed elswhere. The significance of monosomy 11, 14 and 21 etc. were discussed briefly.