Oculocutaneous albinism (OCA) is an autosomal recessive disorder caused by 
either complete lack of or a reduction of melanin biosynthesis in the 
melanocytes. The OCA1A is the most severe type with a complete lack of melanin 
production throughout life, while the milder forms OCA1B, OCA2, OCA3, and OCA4 
show some pigment accumulation over time. Mutations in TYR, OCA2, TYRP1, and 
SLC45A2 are mainly responsible for causing oculocutaneous albinism. Recently, 
two new genes SLC24A5 and C10orf11 are identified that are responsible to cause 
OCA6 and OCA7, respectively. Also a locus has been mapped to the human 
chromosome 4q24 region which is responsible for genetic cause of OCA5. In this 
paper, we summarized the clinical and molecular features of OCA genes. Further, 
we reviewed the screening of pathological mutations of OCA genes and its 
molecular mechanism of the protein upon mutation by in silico approach. We also 
reviewed TYR (T373K, N371Y, M370T, and P313R), OCA2 (R305W), TYRP1 (R326H and 
R356Q) mutations and their structural consequences at molecular level. It is 
observed that the pathological genetic mutations and their structural and 
functional significance of OCA genes will aid in development of personalized 
medicine for albinism patients.