Abstract only Although historically considered to be mitotically inactive, mammalian cardiac muscle cells (cardiomyocytes) are now widely viewed as being capable of at least low levels of homeostatic renewal throughout adulthood. Emerging evidence indicates that the extent to which cardiomyocytes can spontaneously re‐enter the cell cycle correlates with the capacity for cardiac self‐repair and regeneration. Therefore, proliferation rates may offer a predictive tool for investigating the regenerative potential of a species. Here we explore homeostatic cardiomyocyte proliferation in a representative reptile, the leopard gecko ( Eublepharis macularius ) . The gecko heart is characterized by a trabeculated, spongy‐like ventricular lumen. This architecture is also seen in species capable of cardiac regeneration (such as zebrafish), as it provides an increased surface area for diffusion with a decreased reliance on coronary circulation. To assess cardiac cell proliferation, we employed a short duration bromodeoxyurdine (BrdU) pulse‐chase experiment (2 day pulse, 7 day chase), and immunostained for the S phase marker proliferating cell nuclear antigen (PCNA) and the mitotic marker phosphorylated histone H3 (pHH3). We determined that cardiac cells of the gecko heart continually proliferate, even into adulthood. Using double immunofluorescence, we then co‐localized the cardiomyocyte marker myosin heavy chain (MHC) with each of PCNA and pHH3. We found that ~10% of cardiomyocytes have entered the synthesis phase (MHC+/PCNA+), while ~0.5% are mitotically active (MHC+/pHH3+). Next, we performed a long duration BrdU pulse‐chase experiment (7 day pulse, 140 day chase). Unexpectedly, we observed long‐term label‐retaining (= slow cycling) cells throughout the ventricular myocardium. These data suggest that the gecko heart contains populations of both constitutively active and comparatively quiescent cells. Our results combined with a trabeculated ventricular architecture point towards the gecko as an excellent candidate to study cardiac self‐repair and regeneration. Support or Funding Information Natural Sciences and Engineering Research Council (NSERC) Discovery Grant 400358