Forgetting of memory is important for animals to survive in the continuously changing environments. If we cannot forget memory, we will encounter various kinds of problem. For example, new memories may stand in opposition to old memories, and a lot of memories filled in our brain may disturb learning new information. In this study, we analyzed the forgetting of the memory for the diacetyl adaptation in C. elegans, whose neural system is simple and is well understood. In ^{C. elegans}, TIR-1/JNK-1 pathway regulates the secretion of a neural signal from AWC neurons to accelerate forgetting. TIR-1/JNK-1 pathway regulates a neural signal that affects the AWA neurons sensing diacetyl. However, the downstream components of TIR-1/JNK-1 pathway remain unclear. To identify genes that negatively regulate the forgetting of the memory at the downstream of TIR-1/JNK-1 pathway, we focused ceh-36 mutant, in which AWC neurons lose their specific function. The loss of the functional AWC neurons in ceh-36 causes the longer retention of the memory, because the forgetting signals may not be secreted. We mutagenized ceh-36 mutant by ethyl methane sulfate, and screened suppressor mutants of ceh-36, which show the normal retention of diacetyl adaptation. For the efficient screening of the suppressor mutants, we developed a new screening method, in which, we used Cu^{2+ will support the study of forgetting of memory. We plan to investigate this mutation for identifying the genes that affect forgetting.}