For instance, the type and/or position of LYST mutations are likely to influence the genotype-phenotype correlation and thus the disease manifestations.22, 33, 79, 80 Overexpression of exocytic vesicle effectors (ie, Rab27a, Munc13-4, or Slp3) has also been shown to restore degranulation by CTLs from patients with CHS, an effect attributed to the compromised delivery of those effector proteins to lytic granules in CTLs, resulting in a fusion-incompetent state.63 This evidence concerns the gene RAB27A and Chédiak-Higashi syndrome.