We propose a model (Fig. 7) in which an equilibrium telomere length in germ cell progenitors is disrupted even in the context of reduced function of LARP7, haploinsufficiency in the telomeric aspects of LARP7 function, while LARP7’s other functions are sufficiently robust that the developmental phenotypes of Alazami syndrome are recessive in nature. The gene discussed is LARP7; the disease is microcephalic primordial dwarfism, Alazami type.