Therefore, disturbances of α-tubulin, inversin, DVL-1, Wnt5a/b, and β-catenin found in diseased yotari kidneys might be the underlying pathological mechanism and a result of the switch from non-canonical to canonical Wnt pathway in the developing and postnatal kidneys, resulting in CAKUT and impairment of kidney function, such as chronic kidney failure. This evidence concerns the gene INVS and congenital anomaly of kidney and urinary tract.