In 2006, researchers uncovered that primary palmar hyperhidrosis, referring to excess sweating on the palms of the hands and feet, maps to the gene locus 14q11.2-q13. After this discovery, further research was conducted to examine if primary<unk>  maps back to the same locus. In addition, researchers wanted to see if other previously unknown genes were responsible for different phenotypes among individuals with hyperhidrosis. Based on previous research using mice and rats, researchers looked towards the role of aquaporin 5 (AQP5), a water channel protein, in human individuals with primary<unk> . AQP5 has been identified as a candidate gene in many hyperhidrosis studies. Using a family that had members with primary<unk> , researchers found that there was no connection between primary<unk>  and AQP5. There was also no significant connection between the gene 14q11.2-q13 locus, which was linked to primary palmar hyperhidrosis, and primary<unk>  in this family. Due to the inconclusive findings in the study, the question as to what are the genes and proteins that play a significant role in primary<unk>  still remains. The expression of the AQP5 protein and AQP5 mRNA was significantly higher in a patient group in comparison to the control group. In 2011, using a control group (individuals without primary<unk>  and a patient group (individuals with primary<unk>  researchers found that there was no difference between the number of sweat coils in the axillary sweat glands. This indicates that there is nothing morphologically different between individuals with and without primary<unk> . The discrepancies between the studies above call on further studies to confirm or deny the role of AQP5, and the role of other proteins, in hyperhidrosis. Beyond looking at the genes and individual proteins that play a role in primary<unk> , researchers have looked at the patterns of heredity for this trait. In a 2003 study, using multiple families, researchers found that primary<unk>  was not a sex-linked gene, since male-to-male transmission was seen in multiple families. Instead evidence supported an autosomal dominant pattern of inheritance with an incomplete disease penetrance. 21 patients in this study reported a positive family history of hyperhidrosis (62%). Researchers were able to uncover this by creating pedigrees of all the participants in the study. Not every member of the pedigree exhibited forms of hyperhidrosis, which allowed the researchers to track the patterns of inheritance. The findings in this study indicated that primary<unk>  is typically an hereditary disorder.
Focal hyperhidrosis
Acquired idiopathic generalized anhidrosis
Hamartia 
Gustatory hyperhidrosis
Generalized lentiginosis
Oral galvanism
Prepubertal hypertrichosis
Symmastia