Inherited retinal diseases (IRDs) are a group of conditions marked by progressive vision loss caused by rod and cone photoreceptor degeneration. Loss of cone photoreceptor function has the largest impact on the quality of life for people living with IRDs as they mediate daylight vision. However, the mechanisms of cone cell death in IRDs are yet to be fully elucidated, limiting the development of treatment approaches. Using the Pde6c^cpfl1 mouse model of achromatopsia (cone dystrophy), and the rd1 of retinitis pigmentosa (rod-cone dystrophy), this study aimed to investigate common disease mechanisms of primary and secondary cone degeneration, respectively, to identify novel therapeutic targets to prevent cone loss. Single-cell RNAseq (scRNAseq) was used to assess differential gene expression patterns between healthy and IRD cones. It was found that RICTOR, the major component of mTORC2, was inhibited in diseased cones. Increasing the activity of the mTORC2 signalling pathway in vivo through pharmaceutical interventions – treatment with either metformin, AICAR, or SC79 – led to therapeutic effects in photoreceptors. Cone numbers were recovered to wildtype levels in treated Pde6c^cpf1 mice, while cone morphology was improved, and rod photoreceptor death was attenuated in rd1 mice. These findings demonstrate that upregulation of mTORC2 pathway activity is neuroprotective to both cone and rod photoreceptor health and could become a clinically viable treatment approach for different types of IRDs.