Cyanobacteria have evolved to survive stressful environmental changes by regulating growth, however, the underlying mechanism for this is obscure. The ability of chromosomal type II toxin-antitoxin (TA) systems to modulate growth or cell death has been documented in a variety of prokaryotes. A chromosomal mazEaFa locus of Anabaena sp. PCC 7120 has been predicted as a putative mazEF TA system. Here we demonstrate that mazEaFa form a bicistronic operon that is co-transcribed under normal growth conditions. Overproduction of MazFa induced Anabaena growth arrest which could be neutralized by co-expression of MazEa. MazFa also inhibited the growth of Escherichia coli cells, and this effect could be overcome by simultaneous or subsequent expression of MazEa via formation of the MazEa-MazFa complex in vivo, further confirming the nature of the mazEaFa locus as a type II TA system. Interestingly, like most TA systems, deletion of mazEaFa had no effect on the growth of Anabaena during the tested stresses. Our data suggest that mazEaFa, or together with other chromosomal type II TA systems, may promote cells to cope with particular stresses by inducing reversible growth arrest of Anabaena.