I think this topic deserves a fair bit of clarification.
First of all, there are many forms of colorblindness (6 major types, plus several rarer types). This is important because this has direct implications for the discussion of qualia, and probably not in the way you think. Let me explain.
The different kinds of colorblindness are informally described as 'red-green' or 'blue-yellow' or somesuch, but it's better to describe them according to their medical terms. The prefixes 'prot-', 'deuter-', and 'trit-' are used for red, green, and blue photoreceptor molecules, respectively, while the suffixes '-anomaly' and '-anopia' are used of modified or absent forms of these molecules, respectively. So we have, for instance, deuteranomaly, which means 'modified form of the green photoreceptor', or protanopia, which means 'no red photoreceptor'. Deuteranomaly is the most common form of colorblindness.
So what does 'modified form' mean? It means that those people with deuteranomaly have the green photoreceptor, it's just a mutated/defective version which is closer in color sensitivity spectrum to the red photoreceptor than the green photoreceptor in normal people. What this means is that people with deuteranomaly actually do have the 'qualia' for all three colors, it's just that since birth the signals from the red and green photoreceptors to the brain have been mostly identical with very little difference, so the brain never learns to make a distinction between the two. In this case, it seems that just by altering the spectrum so that the difference becomes more pronounced, you can 'cure' colorblindness. In fact there are already special glasses that do this.
But in the case where the person totally lacks one photoreceptor, this isn't possible, because as far as I know they fundamentally lack the requisite neural wiring to get three color channels to the brain (but see below).
Now, these people claim to have a gene therapy that gives people a new set of photoreceptors. That's great, but at the end of the day, all that's being accomplished is that some cone cells are being suppressed or excited. Imagine if you took a photo and added some kind of grainy filter over the photo so that the color spectrum of some of the pixels were altered, but only within the range of colors you can already see - no new colors. Now imagine you permanently saw the world through a camera setup that did this to everything. That's basically what's happening here.
It may really cure colorblindness; I don't know. The brain is weird like that. It could definitely help colorblind people learn to distinguish between colors they previously couldn't. But I don't immediately see how this could cause such people to have a novel color sensation/qualia pop out for them. One way I could be wrong is if the neural circuitry for trichromacy exists but is dormant in such individuals.
One way I could be wrong is if the neural circuitry for trichromacy exists but is dormant in such individuals.
If they have grown up without proper trichromatic neural signals flowing from the retina to the LGN into V1, then V1 will have already developed a set of low level gabor features that are bichromatic. To actually see in color, the visual systems of these patients will need to do some relearning.
Based on other known plasticity/rewiring experiments, it seems fairly reasonable that this type of rewiring will occur automatically as a result of new ...
It seems possible that soon there may be a cure for colourblindness. The Mary's Room thought experiment attempts to pin down something about the nature of qualia in a contrived but similar situation, but my feeling is that the actual result of such an experiment would not be obvious. Would we consider the experiment valid if it was performed on somebody familiar with blue and green, but not red?