suprathreshold mf-ERG signals were still not present at 16 weeks post-injection (Fig. 1c, inset). After GFP fluorescence became robust, the red light mf-ERG, which indicates responses from the introduced L-opsin, showed highly increased response amplitudes in two areas (Fig. 1c) corresponding to locations of subretinal injections (Fig. 1d). The two dichromatic monkeys who participated in behavioural tests of colour vision were treated with L-opsin-coding virus only. Although the elongated pattern produced by two injections in Fig. 1c, d allowed mf-ERG validation, the treatment goal was to produce a homogeneous region, as resulted from three injections shown in Fig. 1f, in which the highest mf-ERG response covered about 80u of the central retina—roughly the area for which humans have good red–green discrimination. These results demonstrate that gene therapy changed the spectral sensitivity of a subset of the cones. A priori, there were two possibilities for how a change in spectral sensitivity might change colour vision behaviour. First, animals may have an increase in sensitivity to long-wavelength light, but if the neural circuitry for extracting colour information from the nascent ‘M 1 L cone’ submosaic was absent, they would remain dichromatic—the hallmark of which is having two hues that are indistinguishable from grey (Fig. 2d). The spectral neutral point for individuals that have only S and M cones (for example, monkeys 1 and 2 pre-therapy) occurs near the dominant wavelength of 495 nm. At the limit, an increase in spectral sensitivity would shift the monkeys’ neutral point towards that of individuals with only S and L cones, near the dominant wavelength of 505 nm (Fig. 2d, dashed blue lines). The second, more engaging possibility was that treatment would be sufficient to expand sensory capacity in monkeys, providing them with trichromatic vision. In this case, the animals’ post-therapy results would appear similar to Fig. 2e, obtained from a trichromatic female control monkey