However, these therapeutic interventions cannot completely rescue the renal phenotype, but only ameliorate kidney disease, similarly to the genetic invalidation of Nlrp2. These results highlight the complexity of the physiopathology of cell dysfunction in cystinosis and the multiplicity of activities that the cystinosin protein plays in cells, beyond its function as a cystine/H+ symporter. The gene discussed is NLRP2; the disease is cystinosis.