The distribution in the human genome of the largest family of mobile elements, 
the Alu sequences, has been investigated for the past 30 years, and the vast 
majority of Alu sequences were shown to have the highest density in GC-rich 
isochores. Ten years ago, it was discovered, however, that the small "youngest" 
(most recently transposed) Alu families had a strikingly different distribution 
compared with the "old" families. This raised the question as to how this change 
took place in evolution. We solved what was considered to be a "mystery" by 1) 
revisiting our previous results on the integration and stability of retroviral 
sequences, and 2) assessing the densities of acceptor sites TTTT/AA in isochore 
families. We could conclude 1) that the open state of chromatin structure plays 
a crucial role in allowing not only the initial integration of retroviral 
sequences but also that of the youngest Alu sequences, and 2) that the 
distribution of old Alus can be explained as due to Alu sequences being unstable 
in the GC-poor isochores but stable in the compositionally matching GC-rich 
isochores, again in line with what happens in the case of retroviral sequences.