Multiple signals act in parallel and independently of the niche to regulate the response of GSCs to diet. (A) On a rich diet, neural DILPs directly activate the insulin receptor on GSCs to stimulate PI3K activity, repression of dFOXO, and faster progression through G2, while another diet-controlled signal(s) regulates G1 progression. (B) On a poor diet, reduced insulin signaling results in dFOXO activation, which in turn represses progression through the G2 phase. In addition, regulation by redundant diet-dependent signals ensures that cell cycle progression through both G1 and G2 remains slow when nutritional inputs are limited.