Mycobacterium tuberculosis (Mtb) is an extremely successful pathogen due to its ability to persist, and to latently infect more than one third of the world's population. Indeed, the reason why Mtb is such a successful pathogen is that it can play the waiting game: it lurks - dormant and benign - in the body of the host for decades, before becoming infectious. What is most disturbing is that during their dormant phase, the Mtb mainly lives inside the host's "macrophage" cells, which are supposed to be killing the bacteria. Often, not all bacteria are killed. A small subpopulation - the 'persisters' - manage to hold fort not only against the macrophages, but also against anti-TB drugs, and hence stand their siege for decades together (albeit in a dormant state). How is this possible? What makes these 'persisters' persist? This is what Dr Amit Singh, an Assistant Professor at the Department of Microbiology and Cell Biology at IISc, wishes to decipher. Another microbe that plays the waiting game in the host's immune cells, while infecting millions around the world is HIV-1, human immunodeficiency virus type-1. HIV-1 causes AIDS (acquired immunodeficiency syndrome), a disease which compromises the patient's immune system, and one that still has no complete cure. Like the insidious Mtb, even HIV-1 lies dormant in the host for many years before reactivating itself when the opportune moment of increased oxidative stresses presents itself. But the question remains: Given that the HIV-1 remains latent for many years, what molecular mechanisms initiate the transition from the benign 'sleep mode' of HIV-1, to the virulent 'deathly mode' of HIV-1, and hence to the inevitable escalation towards AIDS?