The hypothesis that the true incidence of c-ALL is relatively uniform throughout the world is not supported by experience in tropical Africa, where ALL is uncommon under five years of age. A high rate of spontaneous somatic mutation in pre-B cells may initiate the development of c-ALL, but its progress could be determined by (i) a leukaemogenic agent causing a second genetic event, (ii) the effects of intense antigenic barrage, either stimulating or suppressing pre-B-cell mitosis, or (iii) genetic determinants. Epidemiological patterns in populations of low, intermediate and high socio-economic status may be classified I-III with increasing incidence of diagnosed T-ALL in children over five years and c-ALL in younger children, and subclassified A and B with decreasing incidence of BL. There may be two forms of AML, one similar to that seen in industrialized countries, the other occurring at high prevalence in African children of low socio-economic status, often presenting with chloroma, and perhaps associated with immune suppression secondary to malnutrition, malaria and other intercurrent infections. Uncontrolled exposure to petroleum and other chemicals, and the use of alkylating agents in treatment of neoplasms in young patients could emerge as important causes of ANLL in Africa. There are two varieties of CLL also, one similar to that seen in the western world, the other prevalent in adults below 45 years of age, especially women: transmission of a leukaemogenic agent is postulated, to which women are more susceptible due to immunosuppression during normal pregnancy. The human population and some subhuman primates of subSaharan Africa are the largest reservoir of HTLV-1, which shows association with B-CLL over 50 years of age and ATL.