In particular, zebrafish larvae engineered by CRISPR-Cas9 to lack the C terminus of SHANK3 (i.e. homozygous or heterozygous shank3abΔC loss-of-function mutant models of Phelan-McDermid syndrome) display increased intestinal transit time due to reduced frequency of peristaltic muscular contractions [80]. The gene discussed is SHANK3; the disease is Monosomy 22q13.