The importance of maintaining P-gp expression is evidenced by the association of functional P-gp deficiency with colonic inflammation: single nucleotide polymorphisms affecting P-gp expression or function in humans are linked to IBD [4, 5], and, further, P-gp (mdr1a) knockout mice develop spontaneous colitis that mimics human ulcerative colitis (UC) [6–8]. The gene discussed is PGP; the disease is inflammatory bowel disease.