Mechanistic studies have shown that cancer cells reactivate this pathway upon drug treatment through two different ways: (1) upregulating the cellular level of active Ras, which leads to paradoxical activation of ERK signaling; and (2) alternative splicing of BRAF(V600E) to generate variants with truncated N-terminus, which enhances BRAF(V600E) homodimerization and decreases drug affinity. Here, BRAF is linked to cancer.