While ES (Fy*BES allele; FY*02N.01) phenotype impairs promoter activity in erythroid cells by disrupting a binding site for the GATA-1 erythroid transcription factor [37] and confers complete protection from vivax malaria, low levels of P. vivax infections have been observed in Fy*01N.01 homozygotes [39], which indicates that P. vivax might be evolving escape-variants able to overcome the protective effect of Fy*01N.01/FY*01N.01 or has evolved a Fy-independent RBC invasion pathway or that the GATA-1 SNP does not abolish Fy expression. Here, GATA1 is linked to Plasmodium vivax malaria.