CpG and TpA dinucleotides are underrepresented in the human genome. The CpG 
deficiency is due to the high mutation rate from C to T in methylated CpG's. The 
TpA suppression was thought to reflect a counterselection against TpA's 
destabilizing effect in RNA. Unexpectedly, the TpA and CpG deficiencies vary 
according to the G+C contents of sequences. It has been proposed that the 
variation in CpG suppression was correlated with a particular chromatin 
organization in G+C-rich isochores. Here, we present an improved model of 
dinucleotide evolution accounting for the overlap between successive 
dinucleotides. We show that an increased mutation rate from CpG to TpG or CpA 
induces both an apparent TpA deficiency and a correlation between CpG and TpA 
deficiencies and G+C content. Moreover, this model shows that the ratio of 
observed over expected CpG frequency underestimates the real CpG deficiency in 
G+C-rich sequences. The predictions of our model fit well with observed 
frequencies in human genomic data. This study suggests that previously published 
selectionist interpretations of patterns of dinucleotide frequencies should be 
taken with caution. Moreover, we propose new criteria to identify unmethylated 
CpG islands taking into account this bias in the measure of CpG depletion.