Although mechanisms of drug resistance and increased angiogenesis in molecularly and immunologically heterogeneous tumors are multifactorial, oncogenic miR-210 and -155 (miRs), in addition to HIF1α and HIF2α, are reportedly overexpressed in many advanced cancers, regulating multiple targets involved in tumor growth, mitochondrial function, and response to anticancer therapy [1,2,3,4,5,6,7,8]. This evidence concerns the gene HIF1A and neoplasm.