Hypothalamic NPY neurons are critically involved in the complex processes that regulate feeding and energy homeostasis. Considering this wide range of functions it is conceivable that different populations of Arc NPY neurons exist that specialise to undertake different responsibilities. However, no knowledge exists how these Arc NPY neurons differ from each other, where they are located, what controls them and what they control. By employing RNAscope we show that a specific subset of Arc NPY neurons exist that do not contain AgRP. This is confirmed by the selective deletion of NPY from AgRP neurons in mice. Baseline levels of AgRP mRNA is not altered in the absence of NPY in these neurons and both AgRP and the remaining NPY neurons are responsive to fasting. Interestingly, bodyweight is significantly higher in AgRPcre/+;NPYlox/lox mice compared to AgRPcre/+;NPYlox/+ control mice and this is accompanied by significantly elevated fat mass. There is a strong trend to increased food intake and this combined with the observed significant decrease in energy expenditure and reduced activity level in the AgRPcre/+;NPYlox/lox mice are the likely causes for the observed increase in bodyweight and fat mass. Surprisingly, bone mass which is also known to be strongly influenced by hypothalamic NPY is unaltered in AgRPcre/+;NPYlox/lox mice suggesting this NPY population is not critical for the central control of bone homeostasis. Interestingly, activating non-NPY AgRP neurons with stimulatory DREADDs is still able to increase food intake, which is reversed when employing an inhibitory version. Taken together this suggests that non-AgRP positive NPY neurons fulfil important different function in the control of whole body energy homeostasis. This is significant, since most past and current research investigating hypothalamic NPY function employ AgRP driven Cre-lines, and as such functional contributions of other NPY neuronal population in the Arc have either been missed or overlooked.