Two more recent studes have revealed that the up-regulated expression and function of TRPV1 in bone cancer pain might be attributed to the the presence of tumor tissue-derived endogenous formaldehyde, which enhances TRPV1 expression via mitogen-activated protein kinase and PI3K, but independently on PKC (Han et al., 2012), as well as the regulatory effects of insulin-like growth factor-1 (Li et al., 2014). Here, TRPV1 is linked to neoplasm.