The intestine is a tissue that is known to undergo regeneration, both continuously as part of tissue homeostasis and in response to damage – for example, that induced by bacterial aggression. While many studies have examined how the gut responds to large amounts of pathogenic or opportunistic bacteria, it is unclear how low levels of bacteria might influence gut homeostasis. Here, on p. 808, Armel Gallet and co-workers tackle this issue. They report that small amounts of the opportunistic Gram-positive bacterium Bacillus thuringiensis var. kurstaki induce a mild early stress response mediated by JNK signalling in the Drosophila midgut. This, in turn, induces the proliferation of intestinal stem cells and leads to the accumulation and overcrowding of differentiated intestinal cells (enterocytes). The authors further report that low amounts of ingested bacteria do not trigger apoptosis, whereas larger amounts do. However, they find that a wave of apoptosis is observed days after infection and acts to eliminate the excess enterocytes. Finally, they demonstrate that the Hippo pathway functions cell-autonomously to trigger the removal of supernumerary enterocytes. These findings lead the authors to propose that the mechanisms involved in the response to the ingestion of low amounts of opportunistic bacteria are different to those mediating the ʻregenerative cell deathʼ that occurs following a stronger aggression.