The cone complement contains the types of cones (or their opsins) expressed by an individual. Causes
Color vision deficiencies can be classified as inherited or acquired. Inherited: inherited or congenital/genetic color vision deficiencies are most commonly caused by mutations of the  genes encoding opsin proteins. However, several other genes can also lead to less common and/or more severe forms of color blindness. Acquired: color blindness that is not present at birth, may be caused by chronic illness, accidents, medication, chemical exposure or simply normal ageing processes. Genetics
Color blindness is typically an inherited genetic disorder. The most common forms of colorblindness are associated with the Photopsin genes, but the mapping of the human genome has shown there are many causative mutations that dont directly affect the opsins. Mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man [OMIM]). Genetics of red–green color blindness
By far the most common form of colorblindness is congenital red–green colorblindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. Protanopia and Deuteranopia (Dichromacy) could be caused by either a missing gene, or a mutation that renders the protein fully non-functional. Protanomaly and Deuteranomaly are caused by a mutation of the genes that causes the spectral sensitivity of the associated opsin proteins to shift towards the other.
The main requirement for trichromacy is three cone cell classes that are each sensitive to different wavelengths of light and therefore have different spectral sensitivities. Dichromats only express two cone classes and cone monochromats express one. For each cone missing, one of the opponent channels (red-green and blue-yellow) that are responsible for color discrimination are disabled. This is the mechanism for protanopia, deuteranopia, blue cone monochromacy and tritanopia. Even when there is trichromatic color vision and all three opponent channels are active, the size of an individuals color gamut is determined by the dynamic range of the opponent channels, which can be affected by several factors. One of these factors is the peak wavelengths of the spectral sensitivities of the three cones, namely the spectral distance between two cones contributing to an opponent channel. When this distance is smaller, the dynamic range is smaller and the color gamut is smaller, leading to a color vision deficiency. This is the mechanism for congenital protanomaly and deuteranomaly, though not of tritanomaly. The opponent channels can also be affected by the prevalence of certain cones in the retinal mosaic. The cones are not equally prevalent and not evenly distributed in the retina. When the number of one of these cone types is significantly reduced, this can also lead to or contribute to a color vision deficiency. This is one of the causes of tritanomaly. Simple colored filters can also create mild color vision deficiencies.