Since MM cells were assumed to be resistant to EGFR-TKI due to rare EGFR mutations and frequent mutations of KRAS/NRAS/BRAF downstream of EGFR signaling pathway, and previously reported to be moderate or less sensitive to first/second generation TKI (Gefitinib/Afatinib) in a cellular context of NRAS mutation dependent manner [21], we thus hypothesized to find and validate the drug target of FHND compounds in MM cells that would be explored as new therapeutic directions in anti-myeloma therapies. This evidence concerns the gene EGFR and Miyoshi myopathy.