The folliculitis-like toxicities associated with EGFR blockade for diseases such as colorectal cancer (CRC) [83, 84] correlate with therapeutic efficacy, whereas tumoral resistance to these drugs is predicted by activating KRAS or BRAF mutations that make EGFR signaling redundant; in KRAS/BRAF-wild-type colon cancers, resistance to EGFR blockade may likewise arise from mutations upregulating FGFR2 function [85–87]. This evidence concerns the gene EGFR and colorectal carcinoma.