Although several different hypothesis have been raised to explain the overexpression of HIF1α in PC tumors and cell lines, including gene amplification [44], increased transcription of HIF1α mRNA [45], single nucleotide polymorphisms [46], expression of truncated HIF1α isoforms [19], and tumor hypoxia-dependent stabilization of HIF1α [29], there is no definitive consensus on the mechanism involved. The gene discussed is HIF1A; the disease is pachyonychia congenita.