As bone tumors in H2‐c‐fosLTR mice arise from the osteoblastic lineage (Grigoriadis et al, 1993), we hypothesize that the tumor cell‐intrinsic function of EGFR might be similar to its role in pancreatic ductal adenocarcinoma (PDAC), where EGFR deletion or inhibition was shown to ameliorate KRAS‐driven PDAC (Ardito et al, 2012; Navas et al, 2012). The gene discussed is EGFR; the disease is bone neoplasm.