In a ground-breaking recent study, Li and colleagues provided compelling evidence that the compound acetonide mitigates the loss of RGCs and reduces oxidative stress through the activation of the PI3K/AKT signaling pathway by enhancing the expression of Cav-1 which more specifically further highlights the potential of Cav-1 as a promising endogenous molecule whose impaired function plays a critical role in optic neuropathy and the degeneration of RGCs in glaucoma [131]. The gene discussed is CAV1; the disease is glaucoma.