The exact mechanism of HCQ and CQ toxicity remains unclear. Previously, it was hypothesized that retinal toxicity results from binding of HCQ and CQ to melanin in the retinal pigment epithelium (RPE), thus damaging the overlying photoreceptors and ultimately causing vision loss .Whether the primary effect of antimalarials occurs at the level of the RPE versus the retinal photoreceptors has been debated, however, as newer imaging technology has become available ,Early retinal toxicity is generally asymptomatic, with subtle alterations in foveal pigmentation that are often not evident on routine ophthalmologic examination. As toxicity progresses, classic "bull's eye" maculopathy, representing a ring of parafoveal RPE depigmentation sparing the central fovea, may be noted. Progression leads to increasing visual impairment, symptomatically manifesting as decreased central vision, reduced color vision, reduced night vision, reading difficulties, central scotomata, flashing lights, and increasing visual field defects.