Autophagic cell death (ACD) can be operationally described as cell death with an autophagic component. While most molecular bases of this autophagic component are known, in ACD the mechanism of cell death proper is not well defined, in particular because in animal cells there is poor experimental distinction between what triggers autophagy and what triggers ACD. Perhaps as a consequence, it is often thought that in animal cells a little autophagy is protective while a lot is destructive and leads to ACD, thus that the shift from autophagy to ACD is quantitative. The aim of this article is to review current knowledge on ACD in Dictyostelium, a very favorable model, with emphasis on (1) the qualitative, not quantitative nature of the shift from autophagy to ACD, in contrast to the above, and (2) random or targeted mutations of in particular the following genes: iplA (IP3R), TalB (talinB), DcsA (cellulose synthase), GbfA, ugpB, glcS (glycogen synthase) and atg1. These mutations allowed the genetic dissection of ACD features, dissociating in particular vacuolisation from cell death.