Already in the 1960s, cytogenetic analyses of acute myeloid leukaemia (AML) revealed recurrent losses of a member of the C-group, which included chromosomes 6-12 and X in this pre-banding era, and shortly after the advent of chromosome banding techniques, it was shown that this monosomy in AML in most instances represented a loss of chromosome 7.1 It was soon realised that -7 is the second most frequent numerical abnormality in AML, occurring as a sole change or as part of a complex karyotype in approximately 10% of all cases (https://mitelmandatabase.isb-cgc.org/; accessed 2 November 2020). Firstly, -7 may reflect a predisposition to AML due to a mutated tumour suppressor gene on chromosome 7. Thus, we here show, for the first time, that the retained chromosome 7 in AML and HoL ALL with monosomy 7 is equally often of maternal and paternal origin, hence refuting the hypothesis that retention or loss of imprinted loci on chromosome 7 is the pathogenetically important consequence of monosomy 7 in adult AML and in HoL ALL. The imprinted region on human chromosome 7q32 extends to the carboxypeptidase A gene cluster: an imprinted candidate for Silver-Russell syndrome. [Extracted from the article]