<unk>  has two main causes. *The first cause is isolated enzyme deficiency. The enzyme<unk>  kinase is encoded by the X-chromosome in humans. It acts as a catalyst in the phosphorylation of<unk>  to<unk> -3-phosphate which plays a key role in formation of triacylglycerol (TAG) and fat storage. There is no strict genotype–phenotype correlation in isolated<unk> ; it can be either symptomatic or asymptomatic. Symptomatic means that<unk>  shows symptoms when it persists in the body and asymptomatic means that the no symptoms appear in the body. In this deficiency the genotype is not associated with the phenotype. The presence of certain mutations in genes has no relation with the phenotype i.e. any resulting physical traits or abnormality. Location of the<unk>  Kinase gene on the X chromosome *The second cause is a deletion or mutation of a single gene.<unk>  is described by Mendelian inheritance and is an X-linked recessive trait due to which it occurs mainly in males and occasionally in females.<unk>  results when the<unk>  kinase gene present on the locus Xp21 of the X chromosome is either deleted or mutated. Females have two X chromosomes and males have one X and one Y chromosome. The expression of recessive genes on the X chromosome is different in males and females. This is due to the fact that genes present on the Y chromosome do not pair up with genes on the X chromosome in males. In females the disorder is expressed only when there are two copies of the affected gene present on each X chromosome but since the<unk>  kinase gene is present only on one X chromosome the disorder is not expressed in women. Women have a second good copy that can compensate for the defect on the first copy. On the other hand, males only need a single copy of the recessive gene for the disorder to be expressed. They do not have a second copy that can protect against any defect on the first copy.
Glycerol kinase deficiency
2,4 Dienoyl-CoA reductase deficiency
Holocarboxylase synthetase deficiency
Dolichol kinase deficiency
Mevalonate kinase deficiency
Enolase deficiency
Malonyl-CoA decarboxylase deficiency
Acyl-CoA oxidase deficiency