The present invention relates to provide a non-human animal model unresponsive to a synthetic compound wherein a gene function encoding TLR7 that recognizes an immunopotentiating synthetic compound such as imidazoquinoline lacks on is genomic locus. Whole or part of a gene fragment of a gene site including an intracellular region and a transmembrane region of a TLR7 gene obtained from a mouse gene library is replaced by a plasmid including poly A signal and a marker gene to construct a targeting vector. Then, this targeting vector is linearized and transferred into embryonic stem cells. The target embryonic stem cells wherein the TLR7 gene function is deleted are microinjected into a mouse blastocyst to generate a chimeric mouse. Then, this chimeric mouse is crossed with a wild-type mouse to generate a heterozygote mouse. Next, the heterozygote mice are intercrossed to obtain a TLR7 knockout mouse.