In Plasmodium falciparum, the causative agent of human malaria, the catalytic 
subunit gene of cAMP-dependent protein kinase (Pfpka-c) exists as a single copy. 
Interestingly, its expression appears developmentally regulated, being at higher 
levels in the pathogenic asexual stages than in the sexual forms of parasite 
that are responsible for transmission to the mosquito vector. Within asexual 
parasites, PfPKA activity can be readily detected in schizonts. Similar to 
endogenous PKA activity of noninfected red blood cells, the parasite enzyme can 
be stimulated by cAMP and inhibited by protein kinase inhibitor.Importantly, ex 
vivo treatment of infected erythrocytes with the classical PKA-C inhibitor H89 
leads to a block in parasite growth. This suggests that the PKA activities of 
infected red blood cells are essential for parasite multiplication. Finally, 
structural considerations suggest that drugs targeting the parasite, rather than 
the erythrocyte enzyme, might be developed that could help in the fight against 
malaria.