The expression of the erythroblastic leukemia viral oncogene homolog (ERBB) family is closely linked to tumor progression through the constitutive activation of downstream signaling, such as the epidermal growth factor (EGF) receptor (EGFR) pathway or through a somatic mutation; ERBB expression is enhanced during tumor microenvironment (TME) formation, cancer progression, and drug-resistance [1]. This evidence concerns the gene EGF and neoplasm.