Polycystic ovary syndrome (PCOS) is a common endocrine disease usually accompanied by infertility. In PCOS, granulosa cells (GCs) produce insufficient energy via glycolysis to support proper follicle (egg-releasing sac) development, resulting in a condition called follicular dysplasia. miRNAs in small vesicles (exosomes) within the follicular fluid can regulate GCs, but whether these miRNAs affect GC glycolysis in PCOS is unclear. To find out, a recent study sequenced the RNA in exosomes from clinical follicular fluid samples. Compared to controls, exosomes from patients with PCOS had higher levels of the miRNA miR-143-3p and lower levels of the miRNA miR-155-5p. Glycolysis pathways were also negatively regulated in PCOS exosomes. In vitro, experiments on a KGN cell PCOS model confirmed that miR-143-3p inhibited glycolysis by silencing the gene HK2. miR-155-5p normally blocks miR-143-3p’s activity, so the miR-155-5p downregulation in PCOS permitted miR-143-3p to silence HK2. The resulting glycolysis impairment increased apoptosis through the lactate and ATP pathways, leading to follicular dysplasia. Although clinical studies are needed, the findings reveal two miRNAs that antagonistically regulate follicular dysplasia in PCOS and identify miR-143-3p, miR-155-5p, and HK2 as potential therapeutic targets for this common cause of infertility.