Human malaria is a mosquito-borne infectious disease caused by protozoan parasites of the genus Plasmodium and transmitted by mosquitoes of the genus Anopheles. It is a major cause of disease and poverty in resource-limited countries, particularly in Africa. Plasmodium falciparum is the most prevalent and virulent species. The human malaria parasite, with life stages in both human and the mosquito vector, presents a high degree of phenotypic plasticity, which allows it to respond and to adapt to changing environmental conditions during its life-cycle. The parasites are able to display phenotypic changes throughout development and to adapt, with variability in traits such as morphology, length of the life-cycles and virulence or pathogenesis. This is associated to a tight regulation at the level of transcription, so that genes with identical sequences can be found in different transcriptional states. For example, the variable expression of subsets of proteins, i.e. surface antigens, facilitates the evasion of the host immune responses and the optimization of survival and transmission. Extensive transcriptional regulation during development and adaptation in the malaria parasites is made possible by epigenetic mechanisms and in recent years, the focus in the field has been the study of epigenetic regulation in the human host. However, some processes are still poorly understood. Importantly, there is very little information about phenotypic plasticity and underlying epigenetic mechanisms and regulatory networks in the stages of development in the mosquito, despite transmission and development within the mosquito host being crucial for the biology and virulence of the parasite.